1993
|
Murphy, K. M.; Sweet, M. J.; Ross, I. L.; Hume, D. A. Effects of the tat and nef gene products of human immunodeficiency virus type 1 (HIV-1) on transcription controlled by the HIV-1 long terminal repeat and on cell growth in macrophages (Journal Article) In: Journal of Virology, vol. 67, no. 12, pp. 6956–6964, 1993, ISSN: 0022538X. @article{murphy_effects_1993,
title = {Effects of the tat and nef gene products of human immunodeficiency virus type 1 (HIV-1) on transcription controlled by the HIV-1 long terminal repeat and on cell growth in macrophages},
author = {K. M. Murphy and M. J. Sweet and I. L. Ross and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0027436026&doi=10.1128%2fjvi.67.12.6956-6964.1993&partnerID=40&md5=3db36a5f52cc0fe70be038db647f47e7},
doi = {10.1128/jvi.67.12.6956-6964.1993},
issn = {0022538X},
year = {1993},
date = {1993-01-01},
journal = {Journal of Virology},
volume = {67},
number = {12},
pages = {6956--6964},
abstract = {The RAW264 murine macrophage cell line was used as a model to examine the role of the tat and nef gene products in the transcription regulation of the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) in macrophages. Contrary to claims that the activity of the HIV-1 LTR responds poorly in rodent cells to trans activation by the viral tat gene product, cotransfection of RAW264 cells with a tat expression plasmid in transient transfection assays caused a textgreater20-fold increase in reporter gene expression that was inhibited by mutations in the TAR region. RAW264 cells stably transfected with the tat plasmid displayed similarly elevated HIV-1 LTR- driven reporter gene activity. By contrast to previous reports indicating a negative role for nef in HIV transcription, cotransfection of RAW264 cells with a nef expression plasmid trans activated the HIV-1 LTR driving either a chloramphenicol acetyltransferase or a luciferase reporter gene. The action of nef was specific to the LTR, as expression of nef had no effect on the activity of the simian virus 40, c-fms, urokinase plasminogen activator, or type 5 acid phosphatase promoter. trans-activating activity was also manifested by a frameshift mutant expressing only the first 35 amino acids of the protein. The effects of nef were multiplicative with those of tat gene product and occurred even in the presence of bacterial lipopolysaccharide, which itself activated LTR-directed transcription. Examination of the effects of selected mutations in the LTR revealed that neither the κB sites in the direct repeat enhancer nor the TAR region was required as a cis-acting element in nef action. The action of nef was not species restricted; it was able to trans activate in the human monocyte-like cell line Mono Mac 6. The presence of a nef expression cassette in a neomycin phosphotransferase gene expression plasmid greatly reduced the number of G418-resistant colonies generated in stable transfection of RAW264 cells, and many of the colonies that were formed exhibited very slow growth. The frameshift mutant was also active in reducing colony generation. Given the absence of any effect of the frameshift mutation on nef function, its actions on macrophage growth and HIV transcription are discussed in terms of the role of the N-terminal 30 amino acids and of stable secondary structures in the mRNA.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The RAW264 murine macrophage cell line was used as a model to examine the role of the tat and nef gene products in the transcription regulation of the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) in macrophages. Contrary to claims that the activity of the HIV-1 LTR responds poorly in rodent cells to trans activation by the viral tat gene product, cotransfection of RAW264 cells with a tat expression plasmid in transient transfection assays caused a textgreater20-fold increase in reporter gene expression that was inhibited by mutations in the TAR region. RAW264 cells stably transfected with the tat plasmid displayed similarly elevated HIV-1 LTR- driven reporter gene activity. By contrast to previous reports indicating a negative role for nef in HIV transcription, cotransfection of RAW264 cells with a nef expression plasmid trans activated the HIV-1 LTR driving either a chloramphenicol acetyltransferase or a luciferase reporter gene. The action of nef was specific to the LTR, as expression of nef had no effect on the activity of the simian virus 40, c-fms, urokinase plasminogen activator, or type 5 acid phosphatase promoter. trans-activating activity was also manifested by a frameshift mutant expressing only the first 35 amino acids of the protein. The effects of nef were multiplicative with those of tat gene product and occurred even in the presence of bacterial lipopolysaccharide, which itself activated LTR-directed transcription. Examination of the effects of selected mutations in the LTR revealed that neither the κB sites in the direct repeat enhancer nor the TAR region was required as a cis-acting element in nef action. The action of nef was not species restricted; it was able to trans activate in the human monocyte-like cell line Mono Mac 6. The presence of a nef expression cassette in a neomycin phosphotransferase gene expression plasmid greatly reduced the number of G418-resistant colonies generated in stable transfection of RAW264 cells, and many of the colonies that were formed exhibited very slow growth. The frameshift mutant was also active in reducing colony generation. Given the absence of any effect of the frameshift mutation on nef function, its actions on macrophage growth and HIV transcription are discussed in terms of the role of the N-terminal 30 amino acids and of stable secondary structures in the mRNA. |
Xie, Y.; Gavel, S.; Cassady, A. I.; Stacey, K. J.; Dunn, T. L.; Hume, D. A. The resistance of macrophage‐like tumour cell lines to growth inhibition by lipopolysaccharide and pertussis toxin (Journal Article) In: British Journal of Haematology, vol. 84, no. 3, pp. 392–401, 1993, ISSN: 00071048. @article{xie_resistance_1993,
title = {The resistance of macrophage‐like tumour cell lines to growth inhibition by lipopolysaccharide and pertussis toxin},
author = {Y. Xie and S. Gavel and A. I. Cassady and K. J. Stacey and T. L. Dunn and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0027293141&doi=10.1111%2fj.1365-2141.1993.tb03092.x&partnerID=40&md5=17a039c2f781eabc9fcbe15c1a3938ce},
doi = {10.1111/j.1365-2141.1993.tb03092.x},
issn = {00071048},
year = {1993},
date = {1993-01-01},
journal = {British Journal of Haematology},
volume = {84},
number = {3},
pages = {392--401},
abstract = {Summary. The process of tumorigenesis is frequently associated with resistance to growth inhibition by physiological regulators of normal cells. Murine macrophage‐like cell lines BAC1.2F5, RAW264, J774.1A and PU5/1.8 were resistant to growth inhibition by bacterial lipopolysaccharide (LPS) and pertussis toxin, agents that blocked growth of primary bone marrow‐derived macrophages (BMDM) in the presence of macrophage colony‐stimulating factor (CSF‐1). The resistance of the CSF‐1‐dependent cell line BAC1.2F5 to growth inhibition by pertussis toxin argues against the possibility that pertussis toxin‐sensitive G proteins are essential for the pathway of growth stimulation by CSF‐1. Conversely, these data add further weight to the argument that LPS mediates some of its biological activities by mimicking the action of pertussis toxin and inhibiting G protein function. The resistance of cell lines to LPS and pertussis toxin was not correlated with any alteration in the expression of mRNA encoding any of three pertussis‐toxin sensitive G protein α subunits. The pattern of G protein expression was consistent between primary cells and tumour cells, suggesting that this is a differentiation marker. In particular, Giα2 mRNA was expressed at remarkably high levels in all of the cells. The specificity of LPS resistance was investigated by studying down‐regulation of CSF‐1 binding and induction of protooncogene c‐fos and tumour necrosis factor (TNF) mRNA. BAC1.2F5 cells were LPS‐resistant in each of these assays. In CSF‐1 binding. RAW264 and J774.1A responded in the same way as bone marrow‐derived macrophages but required higher doses of LPS, whereas c‐fos and TNF mRNA were induced in these cells at concentrations that did not inhibit growth. In PU5/1.8 cells, CSF‐1 binding was already very low and was not further down‐regulated, but c‐fos and TNF mRNA was inducible by LPS. By contrast to primary macrophages, the cell lines did not respond to LPS with down‐regulation of c‐fms mRNA, which encodes the CSF‐1 receptor. Hence, the resistance of macrophage‐like tumour cells to LPS and pertussis toxin was specific to the pathways controlling growth, and was correlated with altered regulation of the CSF‐1 receptor. Copyright © 1993, Wiley Blackwell. All rights reserved},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Summary. The process of tumorigenesis is frequently associated with resistance to growth inhibition by physiological regulators of normal cells. Murine macrophage‐like cell lines BAC1.2F5, RAW264, J774.1A and PU5/1.8 were resistant to growth inhibition by bacterial lipopolysaccharide (LPS) and pertussis toxin, agents that blocked growth of primary bone marrow‐derived macrophages (BMDM) in the presence of macrophage colony‐stimulating factor (CSF‐1). The resistance of the CSF‐1‐dependent cell line BAC1.2F5 to growth inhibition by pertussis toxin argues against the possibility that pertussis toxin‐sensitive G proteins are essential for the pathway of growth stimulation by CSF‐1. Conversely, these data add further weight to the argument that LPS mediates some of its biological activities by mimicking the action of pertussis toxin and inhibiting G protein function. The resistance of cell lines to LPS and pertussis toxin was not correlated with any alteration in the expression of mRNA encoding any of three pertussis‐toxin sensitive G protein α subunits. The pattern of G protein expression was consistent between primary cells and tumour cells, suggesting that this is a differentiation marker. In particular, Giα2 mRNA was expressed at remarkably high levels in all of the cells. The specificity of LPS resistance was investigated by studying down‐regulation of CSF‐1 binding and induction of protooncogene c‐fos and tumour necrosis factor (TNF) mRNA. BAC1.2F5 cells were LPS‐resistant in each of these assays. In CSF‐1 binding. RAW264 and J774.1A responded in the same way as bone marrow‐derived macrophages but required higher doses of LPS, whereas c‐fos and TNF mRNA were induced in these cells at concentrations that did not inhibit growth. In PU5/1.8 cells, CSF‐1 binding was already very low and was not further down‐regulated, but c‐fos and TNF mRNA was inducible by LPS. By contrast to primary macrophages, the cell lines did not respond to LPS with down‐regulation of c‐fms mRNA, which encodes the CSF‐1 receptor. Hence, the resistance of macrophage‐like tumour cells to LPS and pertussis toxin was specific to the pathways controlling growth, and was correlated with altered regulation of the CSF‐1 receptor. Copyright © 1993, Wiley Blackwell. All rights reserved |
Yue, X.; Favot, P.; Dunn, T. L.; Cassady, A. I.; Hume, D. A. Expression of mRNA encoding the macrophage colony-stimulating factor receptor (c-fms) is controlled by a constitutive promoter and tissue-specific transcription elongation (Journal Article) In: Molecular and Cellular Biology, vol. 13, no. 6, pp. 3191–3201, 1993, ISSN: 02707306. @article{yue_expression_1993,
title = {Expression of mRNA encoding the macrophage colony-stimulating factor receptor (c-fms) is controlled by a constitutive promoter and tissue-specific transcription elongation},
author = {X. Yue and P. Favot and T. L. Dunn and A. I. Cassady and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0027256018&doi=10.1128%2fMCB.13.6.3191&partnerID=40&md5=abe7f86bf197941e22b74d309ba40346},
doi = {10.1128/MCB.13.6.3191},
issn = {02707306},
year = {1993},
date = {1993-01-01},
journal = {Molecular and Cellular Biology},
volume = {13},
number = {6},
pages = {3191--3201},
abstract = {The gene encoding the receptor for macrophage colony-stimulating factor 1 (CSF-1), the c-fms proto-oncogene, is selectively expressed in immature and mature mononuclear phagocytes and trophoblasts. Exon 1 is expressed only in trophoblasts. Isolation and sequencing of genomic DNA flanking exon 2 of the murine c-fms gene revealed a TATA-less promoter with significant homology to human c-fms. Reverse transcriptase primer extension analysis using exon 2 primers identified multiple clustered transcription initiation sites. Their position was confirmed by RNase protection. The same primer extension products were detected in equal abundance from macrophage or nonmacrophage sources of RNA. c-fms mRNA is acutely down-regulated in primary macrophages by CSF-1, bacterial lipopolysaccharide (LPS), and phorbol myristate acetate (PMA). Each of these agents reduced the abundance of c-fms RNA detectable by primer extension using an exon 3 primer without altering the abundance of presumptive short c-fms transcripts detected with exon 2 primers. Primer extension analysis with an intron 2 primer detected products at greater abundance in nonmacrophages. Templates detected with the intronic primer were induced in macrophages by LPS, PMA, and CSF-1, suggesting that each of the agents caused a shift from full-length c-fms mRNA production to production of unspliced, truncated transcripts. The c-fms promoter functioned constitutively in the RAW264 macrophage cell line, the B-cell line MOPC.31C, and several nonhematopoietic cell lines. Macrophage-specific expression and responsiveness to selective repression by LPS and PMA was achieved by the incorporation of intron 2 into the c-fms promoter-reporter construct. The results suggest that expression of the c-fms gene in macrophages is controlled by sequences in intron 2 that act by regulating transcription elongation.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The gene encoding the receptor for macrophage colony-stimulating factor 1 (CSF-1), the c-fms proto-oncogene, is selectively expressed in immature and mature mononuclear phagocytes and trophoblasts. Exon 1 is expressed only in trophoblasts. Isolation and sequencing of genomic DNA flanking exon 2 of the murine c-fms gene revealed a TATA-less promoter with significant homology to human c-fms. Reverse transcriptase primer extension analysis using exon 2 primers identified multiple clustered transcription initiation sites. Their position was confirmed by RNase protection. The same primer extension products were detected in equal abundance from macrophage or nonmacrophage sources of RNA. c-fms mRNA is acutely down-regulated in primary macrophages by CSF-1, bacterial lipopolysaccharide (LPS), and phorbol myristate acetate (PMA). Each of these agents reduced the abundance of c-fms RNA detectable by primer extension using an exon 3 primer without altering the abundance of presumptive short c-fms transcripts detected with exon 2 primers. Primer extension analysis with an intron 2 primer detected products at greater abundance in nonmacrophages. Templates detected with the intronic primer were induced in macrophages by LPS, PMA, and CSF-1, suggesting that each of the agents caused a shift from full-length c-fms mRNA production to production of unspliced, truncated transcripts. The c-fms promoter functioned constitutively in the RAW264 macrophage cell line, the B-cell line MOPC.31C, and several nonhematopoietic cell lines. Macrophage-specific expression and responsiveness to selective repression by LPS and PMA was achieved by the incorporation of intron 2 into the c-fms promoter-reporter construct. The results suggest that expression of the c-fms gene in macrophages is controlled by sequences in intron 2 that act by regulating transcription elongation. |
1992
|
Lüthe, R.; Hume, D. Rezensionen (Journal Article) In: Deutsche Zeitschrift fur Philosophie, vol. 40, no. 12, pp. 1471–1488, 1992, ISSN: 00121045. @article{luthe_rezensionen_1992,
title = {Rezensionen},
author = {R. Lüthe and D. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84955835260&doi=10.1524%2fdzph.1992.40.12.1471&partnerID=40&md5=ad3c9761e79027a1ca9e7d6d9231c1f0},
doi = {10.1524/dzph.1992.40.12.1471},
issn = {00121045},
year = {1992},
date = {1992-01-01},
journal = {Deutsche Zeitschrift fur Philosophie},
volume = {40},
number = {12},
pages = {1471--1488},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Hume, D.; McGarry, M. P.; Stewart, C. Letter to the editor [1] (Journal Article) In: Journal of Leukocyte Biology, vol. 51, no. 5, pp. 517–518, 1992, ISSN: 07415400. @article{hume_letter_1992,
title = {Letter to the editor [1]},
author = {D. Hume and M. P. McGarry and C. Stewart},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026863939&doi=10.1002%2fjlb.51.5.517&partnerID=40&md5=c307e7139ef7eb8be3c6acae7c18f8c0},
doi = {10.1002/jlb.51.5.517},
issn = {07415400},
year = {1992},
date = {1992-01-01},
journal = {Journal of Leukocyte Biology},
volume = {51},
number = {5},
pages = {517--518},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Warren, H. S.; Hodder, M. J.; Allan, W.; Hume, D. A.; Simeonovic, C. J. Induction of class II major histocompatibility antigens on thyroid, adult pancreatic islet, and fetal proislet allografts (Journal Article) In: Transplantation, vol. 53, no. 4, pp. 834–840, 1992, ISSN: 00411337. @article{warren_induction_1992,
title = {Induction of class II major histocompatibility antigens on thyroid, adult pancreatic islet, and fetal proislet allografts},
author = {H. S. Warren and M. J. Hodder and W. Allan and D. A. Hume and C. J. Simeonovic},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026689213&doi=10.1097%2f00007890-199204000-00025&partnerID=40&md5=711dfb755ab34db66fae694e05235b6d},
doi = {10.1097/00007890-199204000-00025},
issn = {00411337},
year = {1992},
date = {1992-01-01},
journal = {Transplantation},
volume = {53},
number = {4},
pages = {834--840},
abstract = {Cultured BALB/c (H-2d) thyroid, adult pancreatic islet and fetal proislet tissues can be accepted permanently in CBA/H (H-2k) recipients until rejection is triggered by the transfer of antidonor strain activated immune T cells. Class II MHC antigens are not expressed on the accepted grafts and are induced following immune cell transfer, but expression is quantitatively and qualitatively different for the different tissues. Thyroid allografts show intense class II MHC antigen expression early after immune cell transfer and before extensive tissue destruction has occurred. In contrast, adult islet and fetal proislet allografts show patchy and cytoplasmic staining usually associated with areas of tissue destruction. Gamma-interferon treatment of tissues in vitro showed that proislet tissue has a greater capacity for class II MHC antigen induction than adult islet tissue. The differences in the capacity for class II MHC induction by fetal and adult islet tissue may be important in relation to the pathogenesis of autoimmune disease. © 1992 by Williams & Wilkins.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Cultured BALB/c (H-2d) thyroid, adult pancreatic islet and fetal proislet tissues can be accepted permanently in CBA/H (H-2k) recipients until rejection is triggered by the transfer of antidonor strain activated immune T cells. Class II MHC antigens are not expressed on the accepted grafts and are induced following immune cell transfer, but expression is quantitatively and qualitatively different for the different tissues. Thyroid allografts show intense class II MHC antigen expression early after immune cell transfer and before extensive tissue destruction has occurred. In contrast, adult islet and fetal proislet allografts show patchy and cytoplasmic staining usually associated with areas of tissue destruction. Gamma-interferon treatment of tissues in vitro showed that proislet tissue has a greater capacity for class II MHC antigen induction than adult islet tissue. The differences in the capacity for class II MHC induction by fetal and adult islet tissue may be important in relation to the pathogenesis of autoimmune disease. © 1992 by Williams & Wilkins. |
Le, F.; Wilce, P. A.; Hume, D. A.; Shanley, B. C. Involvement of γ‐Aminobutyric Acid and N‐Methyl‐Đ‐Aspartate Receptors in the Inhibitory Effect of Ethanol on Pentylenetetrazole‐Induced c‐fos Expression in Rat Brain (Journal Article) In: Journal of Neurochemistry, vol. 59, no. 4, pp. 1309–1315, 1992, ISSN: 00223042. @article{le_involvement_1992,
title = {Involvement of γ‐Aminobutyric Acid and N‐Methyl‐Đ‐Aspartate Receptors in the Inhibitory Effect of Ethanol on Pentylenetetrazole‐Induced c‐fos Expression in Rat Brain},
author = {F. Le and P. A. Wilce and D. A. Hume and B. C. Shanley},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026670267&doi=10.1111%2fj.1471-4159.1992.tb08442.x&partnerID=40&md5=26f02d7377f60e61f5d0a8a6bd21a79f},
doi = {10.1111/j.1471-4159.1992.tb08442.x},
issn = {00223042},
year = {1992},
date = {1992-01-01},
journal = {Journal of Neurochemistry},
volume = {59},
number = {4},
pages = {1309--1315},
abstract = {Abstract: The expression of c‐fos mRNA in rat brain was induced by intraperitoneal administration of pentylenetetrazole (PTZ) and picrotoxin, which act on the picrotoxin binding site of the γ‐aminobutyric acid‐benzodiazepine (GABA‐BZ) receptor complex, by N‐methyl‐D‐aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors. The actions of PTZ and picrotoxin but not that of NMDA were blocked by ethanol and the NMDA‐receptor antagonist, MK‐801. Ro 15–4513 partially reversed the inhibitory effect of ethanol on PTZ‐induced c‐fos mRNA synthesis. Acute ethanol administration blocked the actions of PTZ and NMDA without affecting the response to kainic acid or caffeine. Taken together, these data suggest that ethanol blocks c‐fos gene activation by noncompetitive antagonists of the GABA‐BZ receptor via actions on both the NMDA and GABA receptors. Copyright © 1992, Wiley Blackwell. All rights reserved},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Abstract: The expression of c‐fos mRNA in rat brain was induced by intraperitoneal administration of pentylenetetrazole (PTZ) and picrotoxin, which act on the picrotoxin binding site of the γ‐aminobutyric acid‐benzodiazepine (GABA‐BZ) receptor complex, by N‐methyl‐D‐aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors. The actions of PTZ and picrotoxin but not that of NMDA were blocked by ethanol and the NMDA‐receptor antagonist, MK‐801. Ro 15–4513 partially reversed the inhibitory effect of ethanol on PTZ‐induced c‐fos mRNA synthesis. Acute ethanol administration blocked the actions of PTZ and NMDA without affecting the response to kainic acid or caffeine. Taken together, these data suggest that ethanol blocks c‐fos gene activation by noncompetitive antagonists of the GABA‐BZ receptor via actions on both the NMDA and GABA receptors. Copyright © 1992, Wiley Blackwell. All rights reserved |
Doyle, A. G.; Halliday, W. J.; Barnett, C. J.; Dunn, T. L.; Hume, D. A. Effect of recombinant human macrophage colony-stimulating factor 1 on immunopathology of experimental brucellosis in mice (Journal Article) In: Infection and Immunity, vol. 60, no. 4, pp. 1465–1472, 1992, ISSN: 00199567. @article{doyle_effect_1992,
title = {Effect of recombinant human macrophage colony-stimulating factor 1 on immunopathology of experimental brucellosis in mice},
author = {A. G. Doyle and W. J. Halliday and C. J. Barnett and T. L. Dunn and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026533283&partnerID=40&md5=5b748cca8e45514566184548f9c9f217},
issn = {00199567},
year = {1992},
date = {1992-01-01},
journal = {Infection and Immunity},
volume = {60},
number = {4},
pages = {1465--1472},
abstract = {Brucella abortus injected into CBA mice replicated primarily in the spleen and liver, reaching a peak bacterial count in both organs about 7 days postinfection. The organism was eliminated from the liver but declined to a chronic phase in the spleen. The infection caused hepatosplenomegaly. An influx of macrophages into the two organs was monitored by quantitative Northern (RNA blot) analysis of the macrophage-specific marker lysozyme mRNA. Lysozyme mRNA was detectable in spleen and increased three- to fourfold during infection. In liver, lysozyme mRNA was initially undetectable, but at about the peak of infection it reached a level comparable to that in the spleen. Macrophage colony-stimulating factor 1 (CSF-1) has been reported to be elevated in the circulation of animals infected with B. abortus and is known to stimulate monocytopoiesis. To investigate the role of CSF-1 in pathogenesis, we studied the effect of further increasing the CSF-1 concentration by administration of recombinant human CSF-1. Since the infection is characterized by several distinct phases, recombinant human CSF- 1 was administered at defined times relative to these phases. Pronounced effects were observed only when CSF-1 administration was begun during the developing acute phase. The consequences were decreased bacterial numbers in the spleen but an increase in the liver, reduced antibody generation, and increased hepatosplenomegaly. A feature of many chronic intracellular infections is immunosuppression. B. abortus caused a substantial diminution of responsiveness of spleen cells to T-cell mitogens, particularly concanavalin A. This action was mimicked by CSF-1 treatment of the animals prior to spleen cell isolation. The results suggest that CSF-1 plays a role in macrophage recruitment in brucellosis and that recruited macrophages contribute to the immunopathology and immunosuppression.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Brucella abortus injected into CBA mice replicated primarily in the spleen and liver, reaching a peak bacterial count in both organs about 7 days postinfection. The organism was eliminated from the liver but declined to a chronic phase in the spleen. The infection caused hepatosplenomegaly. An influx of macrophages into the two organs was monitored by quantitative Northern (RNA blot) analysis of the macrophage-specific marker lysozyme mRNA. Lysozyme mRNA was detectable in spleen and increased three- to fourfold during infection. In liver, lysozyme mRNA was initially undetectable, but at about the peak of infection it reached a level comparable to that in the spleen. Macrophage colony-stimulating factor 1 (CSF-1) has been reported to be elevated in the circulation of animals infected with B. abortus and is known to stimulate monocytopoiesis. To investigate the role of CSF-1 in pathogenesis, we studied the effect of further increasing the CSF-1 concentration by administration of recombinant human CSF-1. Since the infection is characterized by several distinct phases, recombinant human CSF- 1 was administered at defined times relative to these phases. Pronounced effects were observed only when CSF-1 administration was begun during the developing acute phase. The consequences were decreased bacterial numbers in the spleen but an increase in the liver, reduced antibody generation, and increased hepatosplenomegaly. A feature of many chronic intracellular infections is immunosuppression. B. abortus caused a substantial diminution of responsiveness of spleen cells to T-cell mitogens, particularly concanavalin A. This action was mimicked by CSF-1 treatment of the animals prior to spleen cell isolation. The results suggest that CSF-1 plays a role in macrophage recruitment in brucellosis and that recruited macrophages contribute to the immunopathology and immunosuppression. |
Hume, D. A.; Denkins, Y. The deleterious effect of macrophage colony-stimulating factor (CSF-1) on the pathology of experimental candidiasis in mice (Journal Article) In: Lymphokine and Cytokine Research, vol. 11, no. 2, pp. 95–98, 1992, ISSN: 10565477. @article{hume_deleterious_1992,
title = {The deleterious effect of macrophage colony-stimulating factor (CSF-1) on the pathology of experimental candidiasis in mice},
author = {D. A. Hume and Y. Denkins},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026521721&partnerID=40&md5=5842909d7f19c4f6e7e44e0766a21de9},
issn = {10565477},
year = {1992},
date = {1992-01-01},
journal = {Lymphokine and Cytokine Research},
volume = {11},
number = {2},
pages = {95--98},
abstract = {Mice infected with Candida albicans albicans intravenously were treated before or after infection with macrophage colony-stimulating factor (CSF-1) to elevate their circulating monocyte and tissue macrophage counts. Both treatments exacerbated the disease, causing a doubling of the rate of weight loss and leading to significantly earlier death. The results suggest that macrophages play a major role in the pathology of the disease.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Mice infected with Candida albicans albicans intravenously were treated before or after infection with macrophage colony-stimulating factor (CSF-1) to elevate their circulating monocyte and tissue macrophage counts. Both treatments exacerbated the disease, causing a doubling of the rate of weight loss and leading to significantly earlier death. The results suggest that macrophages play a major role in the pathology of the disease. |
1991
|
Cassady, A. I.; Stacey, K. J.; Nimmo, K. A.; Murphy, K. M.; Ahe, D. Von Der; Pearson, D.; Botteri, F. M.; Nagamine, Y.; Hume, D. A. Constitutive expression of the urokinase plasminogen activator gene in murine RAW264 macrophages involves distal and 5′ non-coding sequences that are conserved between mouse and pig (Journal Article) In: Nucleic Acids Research, vol. 19, no. 24, pp. 6839–6847, 1991, ISSN: 03051048. @article{cassady_constitutive_1991,
title = {Constitutive expression of the urokinase plasminogen activator gene in murine RAW264 macrophages involves distal and 5′ non-coding sequences that are conserved between mouse and pig},
author = {A. I. Cassady and K. J. Stacey and K. A. Nimmo and K. M. Murphy and D. Von Der Ahe and D. Pearson and F. M. Botteri and Y. Nagamine and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026338119&doi=10.1093%2fnar%2f19.24.6839&partnerID=40&md5=1354a69e133c146a3e884dcab8a3b8cc},
doi = {10.1093/nar/19.24.6839},
issn = {03051048},
year = {1991},
date = {1991-01-01},
journal = {Nucleic Acids Research},
volume = {19},
number = {24},
pages = {6839--6847},
abstract = {The 5′ flanking regions of the mouse and pig urokinase plasmlnogen activator (uPA) genes were sequenced and sequence homology interrupted by repeat elements was found to extend to - 4.6kb in pig and - 6.6kb in mouse. A transient transfection procedure was devised for the murine macrophage cell line RAW264. Pig uPA promoter-CAT constructs were more active than mouse constructs in this assay. This contrast may Involve sequence differences within 100 bp of the transcription start site. The selective deletion of distal regions of the promoter (textgreater2.6 kb upstream), and of a conserved element, 5′-AGGAGGAAATGAGGTCA- 3′ around - 2 kb greatly reduced the activity of reporter constructs in RAW264 cells. Electrophoretic mobility shift assays using the latter sequence identified a single nuclear protein complex. This element has been referred to as PEA3/AP1-like, but the complex did not comigrate with either AP1 or knownproteins that bind polypurines (including the macrophage-specific factor PU-1) and was not competed by AP1 or polypurine oligonucleotides. uPA promoters contain multiple AP1 and AP2-like DMA sequences, which were recognised by nuclear proteins expressed constitutively in RAW264 cells. They also contain multiple binding sites for NF×B but activated NF×B was not expressed in RAW264 cells. The conserved, transcribed 5′ non-coding sequences were also required for maximal gene expression. Hence, the uPA promoter contains multiple weak cis-acting elements distributed over 7.0 kb 5′ to the translation start site. © 1991 Oxford University Press.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The 5′ flanking regions of the mouse and pig urokinase plasmlnogen activator (uPA) genes were sequenced and sequence homology interrupted by repeat elements was found to extend to - 4.6kb in pig and - 6.6kb in mouse. A transient transfection procedure was devised for the murine macrophage cell line RAW264. Pig uPA promoter-CAT constructs were more active than mouse constructs in this assay. This contrast may Involve sequence differences within 100 bp of the transcription start site. The selective deletion of distal regions of the promoter (textgreater2.6 kb upstream), and of a conserved element, 5′-AGGAGGAAATGAGGTCA- 3′ around - 2 kb greatly reduced the activity of reporter constructs in RAW264 cells. Electrophoretic mobility shift assays using the latter sequence identified a single nuclear protein complex. This element has been referred to as PEA3/AP1-like, but the complex did not comigrate with either AP1 or knownproteins that bind polypurines (including the macrophage-specific factor PU-1) and was not competed by AP1 or polypurine oligonucleotides. uPA promoters contain multiple AP1 and AP2-like DMA sequences, which were recognised by nuclear proteins expressed constitutively in RAW264 cells. They also contain multiple binding sites for NF×B but activated NF×B was not expressed in RAW264 cells. The conserved, transcribed 5′ non-coding sequences were also required for maximal gene expression. Hence, the uPA promoter contains multiple weak cis-acting elements distributed over 7.0 kb 5′ to the translation start site. © 1991 Oxford University Press. |
Breen, F. N.; Hume, D. A.; Weidemann, M. J. Interactions among granulocyte-macrophage colony-stimulating factor, macrophage colony-stimulating factor, and IFN-γ lead to enhanced proliferation of murine macrophage progenitor cells (Journal Article) In: Journal of Immunology, vol. 147, no. 5, pp. 1542–1547, 1991, ISSN: 00221767. @article{breen_interactions_1991,
title = {Interactions among granulocyte-macrophage colony-stimulating factor, macrophage colony-stimulating factor, and IFN-γ lead to enhanced proliferation of murine macrophage progenitor cells},
author = {F. N. Breen and D. A. Hume and M. J. Weidemann},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0025871906&partnerID=40&md5=54399d021c5deb6dcab8d94c8864e92d},
issn = {00221767},
year = {1991},
date = {1991-01-01},
journal = {Journal of Immunology},
volume = {147},
number = {5},
pages = {1542--1547},
abstract = {This report examines the actions of IFN-γ on monocytopoiesis in murine liquid and semisolid bone marrow cultures. The proliferative response of bone marrow cells to macrophage CSF and granulocyte-macrophage CSF was assayed by measuring [3H]TdR uptake in a range of mouse strains. No interstrain difference in kinetics was observed for CSF-1 action, but GM-CSF acted significantly more rapidly on C57B1/6, Swiss, and to a lesser extent A/J mice than on BALB/c or CBA. IFN-γ inhibited [3H]TdR incorporation elicited by CSF-1, and to a much lesser extent, GM-CSF. When the two CSF were added together, the effects were not additive; in fact, the response was the same as that seen with GM-CSF alone. When IFN-γ was also added, the response was restored to the level seen with CSF-1 alone. In essence, the inhibitory actions of GM-CSF and IFN-γ were mutually exclusive. The mechanism of these actions was investigated using colony assays. As expected, CSF-1 caused the formation of pure macrophage colonies, whereas GM-CSF stimulated production of macrophage, granulocyte, and mixed granulocyte macrophage colonies. When the two CSF were added in combination, the total colony count was greater than with either alone, but less than additive. The number of pure macrophage colonies was reduced to the number seen with GM-CSF alone. IFN-γ reduced the number of colonies in the presence of CSF-1, but slightly increased the number with GM-CSF. In the presence of both CSF, IFN-γ increased the colony count by around 25 to 40%, so that the numbers were greater than the combined total of CSF-1 plus GM-CSF added separately. Similar results were obtained in all mouse strains tested. The results suggest that the thymidine uptake data reflect changes in the number of progenitor cells responding rather than changes in cell cycle time. The results are discussed in terms of the possibility that coadministration of GM-CSF and CSF-1 could ameliorate the myelosuppressive actions of IFN-γ in vivo, leading to more effective use of this agent as a biologic response modifier.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
This report examines the actions of IFN-γ on monocytopoiesis in murine liquid and semisolid bone marrow cultures. The proliferative response of bone marrow cells to macrophage CSF and granulocyte-macrophage CSF was assayed by measuring [3H]TdR uptake in a range of mouse strains. No interstrain difference in kinetics was observed for CSF-1 action, but GM-CSF acted significantly more rapidly on C57B1/6, Swiss, and to a lesser extent A/J mice than on BALB/c or CBA. IFN-γ inhibited [3H]TdR incorporation elicited by CSF-1, and to a much lesser extent, GM-CSF. When the two CSF were added together, the effects were not additive; in fact, the response was the same as that seen with GM-CSF alone. When IFN-γ was also added, the response was restored to the level seen with CSF-1 alone. In essence, the inhibitory actions of GM-CSF and IFN-γ were mutually exclusive. The mechanism of these actions was investigated using colony assays. As expected, CSF-1 caused the formation of pure macrophage colonies, whereas GM-CSF stimulated production of macrophage, granulocyte, and mixed granulocyte macrophage colonies. When the two CSF were added in combination, the total colony count was greater than with either alone, but less than additive. The number of pure macrophage colonies was reduced to the number seen with GM-CSF alone. IFN-γ reduced the number of colonies in the presence of CSF-1, but slightly increased the number with GM-CSF. In the presence of both CSF, IFN-γ increased the colony count by around 25 to 40%, so that the numbers were greater than the combined total of CSF-1 plus GM-CSF added separately. Similar results were obtained in all mouse strains tested. The results suggest that the thymidine uptake data reflect changes in the number of progenitor cells responding rather than changes in cell cycle time. The results are discussed in terms of the possibility that coadministration of GM-CSF and CSF-1 could ameliorate the myelosuppressive actions of IFN-γ in vivo, leading to more effective use of this agent as a biologic response modifier. |
Le, F.; Wilce, P. A.; Cassady, I.; Hume, D. A.; Shanley, B. C. Acute administration of ethanol suppresses pentylenetetrazole-induced c-fos expression in rat brain. (Journal Article) In: Alcohol and alcoholism (Oxford, Oxfordshire). Supplement., vol. 1, pp. 211–214, 1991, ISSN: 13586173. @article{le_acute_1991,
title = {Acute administration of ethanol suppresses pentylenetetrazole-induced c-fos expression in rat brain.},
author = {F. Le and P. A. Wilce and I. Cassady and D. A. Hume and B. C. Shanley},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026379601&partnerID=40&md5=4c999b5dd5191d6514a6f165be8bb67b},
issn = {13586173},
year = {1991},
date = {1991-01-01},
journal = {Alcohol and alcoholism (Oxford, Oxfordshire). Supplement.},
volume = {1},
pages = {211--214},
abstract = {The effect of acute ethanol administration on pentylenetetrazole-induced c-fos expression in rat brain was studied. Pentylenetetrazole induced the rapid and transient expression of c-fos mRNA in rat brain. Maximal induction at a dose of 30 mg/kg was detected within 30 min and persisted for 60 min. Thereafter c-fos gene expression decreased to control levels by 180 min. No increase in c-fos mRNA was evident at doses of pentylenetetrazole textless or = 20 mg/kg, whereas maximal elevation was seen at 30 or 40 mg/kg. This action was inhibited by acute ethanol treatment (blood alcohol level textgreater or = 100 mg/dl). Acute ethanol treatment alone had no effect on c-fos gene expression.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The effect of acute ethanol administration on pentylenetetrazole-induced c-fos expression in rat brain was studied. Pentylenetetrazole induced the rapid and transient expression of c-fos mRNA in rat brain. Maximal induction at a dose of 30 mg/kg was detected within 30 min and persisted for 60 min. Thereafter c-fos gene expression decreased to control levels by 180 min. No increase in c-fos mRNA was evident at doses of pentylenetetrazole textless or = 20 mg/kg, whereas maximal elevation was seen at 30 or 40 mg/kg. This action was inhibited by acute ethanol treatment (blood alcohol level textgreater or = 100 mg/dl). Acute ethanol treatment alone had no effect on c-fos gene expression. |
Abd, A. -H. A.; Savage, N. W.; Halliday, W. J.; Hume, D. A. The role of macrophages in experimental arthritis induced by Streptococcus agalactiae sonicate: Actions of macrophage colony-stimulating factor (CSF-1) and other macrophage-modulating agents (Journal Article) In: Lymphokine and Cytokine Research, vol. 10, no. 1-2, pp. 43–50, 1991, ISSN: 02776766. @article{abd_role_1991,
title = {The role of macrophages in experimental arthritis induced by Streptococcus agalactiae sonicate: Actions of macrophage colony-stimulating factor (CSF-1) and other macrophage-modulating agents},
author = {A. -H. A. Abd and N. W. Savage and W. J. Halliday and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0025812185&partnerID=40&md5=36572b9ac2df826b7974f3c7adc64f24},
issn = {02776766},
year = {1991},
date = {1991-01-01},
journal = {Lymphokine and Cytokine Research},
volume = {10},
number = {1-2},
pages = {43--50},
abstract = {Intraperitoneal injection of Streptococcus agalactiae sonicated cells into Wistar rats causes a chronic relapsing polyarthritis resembling human rheumatoid arthritis. We report evidence favoring a role for macrophages in the pathology of this disease. S. agalactiae injected ip induced a high level of tumor necrosis factor release by peritoneal macrophages isolated subsequently, and had a similar effect when added to control peritoneal macrophages in culture. Ia antigen was induced on macrophages in both the peritoneum and affected joints following S. agalactiae injection. The role of macrophages in the disease process was studied by treating animals prior to S. agalactiae injection with varying concentrations of bacterial lipopolysaccharide (LPS), silica, and carrageenan, agents known to have a biphasic effect on macrophage function. They aggravated the pathology at low doses but prevented the disease at high doses. The most specific alteration of macrophage levels was achieved by injection of recombinant human macrophage colony-stimulating factor (CSF-1). Treatment with CSF-1 early in the disease lead to significant worsening of the pathology. Administration of CSF-1 after 2 weeks reactivated the disease and extended the chronic phase. These data in combination with previous findings are consistent with nonimmune, macrophage-mediated pathology for this model of arthritis. The results have implications for therapeutic application of CSF-1.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Intraperitoneal injection of Streptococcus agalactiae sonicated cells into Wistar rats causes a chronic relapsing polyarthritis resembling human rheumatoid arthritis. We report evidence favoring a role for macrophages in the pathology of this disease. S. agalactiae injected ip induced a high level of tumor necrosis factor release by peritoneal macrophages isolated subsequently, and had a similar effect when added to control peritoneal macrophages in culture. Ia antigen was induced on macrophages in both the peritoneum and affected joints following S. agalactiae injection. The role of macrophages in the disease process was studied by treating animals prior to S. agalactiae injection with varying concentrations of bacterial lipopolysaccharide (LPS), silica, and carrageenan, agents known to have a biphasic effect on macrophage function. They aggravated the pathology at low doses but prevented the disease at high doses. The most specific alteration of macrophage levels was achieved by injection of recombinant human macrophage colony-stimulating factor (CSF-1). Treatment with CSF-1 early in the disease lead to significant worsening of the pathology. Administration of CSF-1 after 2 weeks reactivated the disease and extended the chronic phase. These data in combination with previous findings are consistent with nonimmune, macrophage-mediated pathology for this model of arthritis. The results have implications for therapeutic application of CSF-1. |
1990
|
Hume, D. Macrophage colony-stimulating factor (Journal Article) In: Today's Life Science, vol. 2, no. 6, pp. 20–22+28, 1990, ISSN: 10336893. @article{hume_macrophage_1990,
title = {Macrophage colony-stimulating factor},
author = {D. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0024991735&partnerID=40&md5=999241996474c6398c78e0fa7774b03e},
issn = {10336893},
year = {1990},
date = {1990-01-01},
journal = {Today's Life Science},
volume = {2},
number = {6},
pages = {20--22+28},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Pavli, P.; Woodhams, C. E.; Doe, W. F.; Hume, D. A. Isolation and characterization of antigen-presenting dendritic cells from the mouse intestinal lamina propria (Journal Article) In: Immunology, vol. 70, no. 1, pp. 40–47, 1990, ISSN: 00192805. @article{pavli_isolation_1990,
title = {Isolation and characterization of antigen-presenting dendritic cells from the mouse intestinal lamina propria},
author = {P. Pavli and C. E. Woodhams and W. F. Doe and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0025216095&partnerID=40&md5=c95e57d62cfab7612de1e02b4bf688f4},
issn = {00192805},
year = {1990},
date = {1990-01-01},
journal = {Immunology},
volume = {70},
number = {1},
pages = {40--47},
abstract = {A method was developed for the isolation of antigen-presenting dendritic cells, and macrophages, from mouse intestinal lamina propria and Peyer's patches. Peyer's patches, and the lamina propria of both the small and large intestine, contained cells with potent stimulatory activity in the allogenic mixed leucocyte reaction. These cells were separated from macrophages by fibronectin adherence and further enriched by density centrifugation. The isolated stimulatory cells expressed high levels of class II major histocompatibility complex (MHC) antigens, and resembled splenic dendritic cells in both morphology and function. Macrophages were recovered from the lamina propria but not Peyer's patches. These cells also expressed class II MHC antigens, but failed to stimulate the mixed leucocyte reaction and, instead, induced indomethacin-sensitive suppression.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
A method was developed for the isolation of antigen-presenting dendritic cells, and macrophages, from mouse intestinal lamina propria and Peyer's patches. Peyer's patches, and the lamina propria of both the small and large intestine, contained cells with potent stimulatory activity in the allogenic mixed leucocyte reaction. These cells were separated from macrophages by fibronectin adherence and further enriched by density centrifugation. The isolated stimulatory cells expressed high levels of class II major histocompatibility complex (MHC) antigens, and resembled splenic dendritic cells in both morphology and function. Macrophages were recovered from the lamina propria but not Peyer's patches. These cells also expressed class II MHC antigens, but failed to stimulate the mixed leucocyte reaction and, instead, induced indomethacin-sensitive suppression. |
Breen, F. N.; Hume, D. A.; Weidemann, M. J. The effects of interleukin 3 (IL‐3) on cells responsive to macrophage colony‐stimulating factor (CSF‐1) in liquid murine bone marrow culture (Journal Article) In: British Journal of Haematology, vol. 74, no. 2, pp. 138–145, 1990, ISSN: 00071048. @article{breen_effects_1990,
title = {The effects of interleukin 3 (IL‐3) on cells responsive to macrophage colony‐stimulating factor (CSF‐1) in liquid murine bone marrow culture},
author = {F. N. Breen and D. A. Hume and M. J. Weidemann},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0025038079&doi=10.1111%2fj.1365-2141.1990.tb02556.x&partnerID=40&md5=e0acd49cd452e292f0d425e6193a71e0},
doi = {10.1111/j.1365-2141.1990.tb02556.x},
issn = {00071048},
year = {1990},
date = {1990-01-01},
journal = {British Journal of Haematology},
volume = {74},
number = {2},
pages = {138--145},
abstract = {We have examined variation between inbred mouse strains in the proliferative response of bone marrow cells in liquid culture to macrophage colony‐stimulating factor (CSF‐1) and interleukin 3 (IL‐3). In all mouse strains, thymidine incorporation was stimulated by CSF‐1 and, after an initial lag period, it reached a peak on day 5. In contrast, two mouse strains, A/J and Balb c, had much lower proliferative responses to IL‐3 than did the other strains. In A/J there was no increase in thymidine incorporation above the initial baseline, although the fall in incorporation seen in the absence of any added growth factor was prevented. IL‐3 also presented the loss of CSF‐1 responsiveness observed when A/J bone marrow cells were incubated in medium alone. The lag phase in the response to CSF‐1 was progressively abolished following IL‐3 pre‐treatment. Thus, the data with A/J mice separate two distinct activities of IL‐3 and show that proliferation is not required for the synergistic effect exerted by IL‐3 on CSF‐1‐stimulated macrophage generation from bone marrow. In strains in which IL‐3 alone was able to stimulate proliferation, its action was not additive with that of CSF‐1, and addition of both factors together did not overcome the lag phase. This suggests that the two factors act on the same cell population, and that the known synergistic effect of IL‐3 on macrophage colony formation in soft agar does not result from an increase in the initial rate of proliferation. The possibility that the combination of factors might alter the duration of the growth response in vivo is discussed. Copyright © 1990, Wiley Blackwell. All rights reserved},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
We have examined variation between inbred mouse strains in the proliferative response of bone marrow cells in liquid culture to macrophage colony‐stimulating factor (CSF‐1) and interleukin 3 (IL‐3). In all mouse strains, thymidine incorporation was stimulated by CSF‐1 and, after an initial lag period, it reached a peak on day 5. In contrast, two mouse strains, A/J and Balb c, had much lower proliferative responses to IL‐3 than did the other strains. In A/J there was no increase in thymidine incorporation above the initial baseline, although the fall in incorporation seen in the absence of any added growth factor was prevented. IL‐3 also presented the loss of CSF‐1 responsiveness observed when A/J bone marrow cells were incubated in medium alone. The lag phase in the response to CSF‐1 was progressively abolished following IL‐3 pre‐treatment. Thus, the data with A/J mice separate two distinct activities of IL‐3 and show that proliferation is not required for the synergistic effect exerted by IL‐3 on CSF‐1‐stimulated macrophage generation from bone marrow. In strains in which IL‐3 alone was able to stimulate proliferation, its action was not additive with that of CSF‐1, and addition of both factors together did not overcome the lag phase. This suggests that the two factors act on the same cell population, and that the known synergistic effect of IL‐3 on macrophage colony formation in soft agar does not result from an increase in the initial rate of proliferation. The possibility that the combination of factors might alter the duration of the growth response in vivo is discussed. Copyright © 1990, Wiley Blackwell. All rights reserved |
Abd, A. -H. A.; Hume, D. A.; Halliday, W. J.; Davis, G. H. G. Immunopathological investigations during the course of arthritis induced in rats by Streptococcus agalactiae (Journal Article) In: Medical Microbiology and Immunology, vol. 179, no. 1, pp. 13–23, 1990, ISSN: 03008584. @article{abd_immunopathological_1990,
title = {Immunopathological investigations during the course of arthritis induced in rats by Streptococcus agalactiae},
author = {A. -H. A. Abd and D. A. Hume and W. J. Halliday and G. H. G. Davis},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0025015231&doi=10.1007%2fBF00190146&partnerID=40&md5=1c2c6ae8d0a278d0979cb6e47c33ddcf},
doi = {10.1007/BF00190146},
issn = {03008584},
year = {1990},
date = {1990-01-01},
journal = {Medical Microbiology and Immunology},
volume = {179},
number = {1},
pages = {13--23},
abstract = {A large single intraperitoneal injection of sonicated cells of Streptococcus agalactiae O90R induced polyarthritis in Wistar rats. The arthritis reaction score was monitored according to redness, edema, severity and deformity of rat ankle and wrist joints. The inflammation of joints was confirmed by radiology and histology. Acute arthritis was initiated within 48 h and the chronic form continued for more than 30 days. Although serum immunoglobulin was elevated within 48 h, anti-streptococcal antibody was detected only at later times (by enzyme-linked immunosorbent assay and Arthus-type hypersensitivity reactions) and neither serum nor splenocytes of arthritic rats were able to transfer disease to susceptible, normal rats. From these observations and the finding of streptococcal antigen in joint macrophages (by immunogold labelling) we conclude that arthritis is related to persistent streptococcal fragments rather than to antibody or immune complexes. © 1990, Springer-Verlag. All rights reserved.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
A large single intraperitoneal injection of sonicated cells of Streptococcus agalactiae O90R induced polyarthritis in Wistar rats. The arthritis reaction score was monitored according to redness, edema, severity and deformity of rat ankle and wrist joints. The inflammation of joints was confirmed by radiology and histology. Acute arthritis was initiated within 48 h and the chronic form continued for more than 30 days. Although serum immunoglobulin was elevated within 48 h, anti-streptococcal antibody was detected only at later times (by enzyme-linked immunosorbent assay and Arthus-type hypersensitivity reactions) and neither serum nor splenocytes of arthritic rats were able to transfer disease to susceptible, normal rats. From these observations and the finding of streptococcal antigen in joint macrophages (by immunogold labelling) we conclude that arthritis is related to persistent streptococcal fragments rather than to antibody or immune complexes. © 1990, Springer-Verlag. All rights reserved. |
1989
|
Hume, D. A.; Nayar, R. Encapsulation is not involved in the activities of recombinant gamma interferon associated with multilamellar phospholipid liposomes on murine bone marrow-derived macrophages (Journal Article) In: Lymphokine Research, vol. 8, no. 4, pp. 415–425, 1989, ISSN: 02776766. @article{hume_encapsulation_1989,
title = {Encapsulation is not involved in the activities of recombinant gamma interferon associated with multilamellar phospholipid liposomes on murine bone marrow-derived macrophages},
author = {D. A. Hume and R. Nayar},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0024452163&partnerID=40&md5=1782a2b2a647aeed37cacedf9307eb68},
issn = {02776766},
year = {1989},
date = {1989-01-01},
journal = {Lymphokine Research},
volume = {8},
number = {4},
pages = {415--425},
abstract = {Bone marrow-derived macrophages were used to study the mechanism of action of recombinant gamma interferon associated with multilamellar phospholipid liposomes. Gamma interferon associated with liposomes caused an inhibition of [3H]-thymidine uptake induced by macrophage colony-stimulating factor (CSF-1), and primed macrophages for subsequent induction of tumoricidal activity by bacterial lipopolysaccharide (LPS). The liposomes were equally active whether the gamma interferon was added before, or after vesicle formation. The result suggested that significant biologically active gamma interferon was bound to the outside of the vesicles. Interferon binding to liposomes was confirmed using radiolabelled ligand. The liposomes themselves were found to be biologically active in promoting proliferation and in acting synergistically to prime cytotoxicity. Vesicles that contained both phosphatidylethanolamine and phosphatidyl-serine or succinylated phosphatidylethanolamine were most active. Such vesicles were found to be internalised rapidly by bone marrow-derived macrophages. Thus, encapsulation of ligand, and internalisation into cytoplasm, do not appear to be involved in the action of liposome-associated gamma interferon. On the other hand, the liposomes may contribute in other ways to improving the therapeutic potential of gamma interferon.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Bone marrow-derived macrophages were used to study the mechanism of action of recombinant gamma interferon associated with multilamellar phospholipid liposomes. Gamma interferon associated with liposomes caused an inhibition of [3H]-thymidine uptake induced by macrophage colony-stimulating factor (CSF-1), and primed macrophages for subsequent induction of tumoricidal activity by bacterial lipopolysaccharide (LPS). The liposomes were equally active whether the gamma interferon was added before, or after vesicle formation. The result suggested that significant biologically active gamma interferon was bound to the outside of the vesicles. Interferon binding to liposomes was confirmed using radiolabelled ligand. The liposomes themselves were found to be biologically active in promoting proliferation and in acting synergistically to prime cytotoxicity. Vesicles that contained both phosphatidylethanolamine and phosphatidyl-serine or succinylated phosphatidylethanolamine were most active. Such vesicles were found to be internalised rapidly by bone marrow-derived macrophages. Thus, encapsulation of ligand, and internalisation into cytoplasm, do not appear to be involved in the action of liposome-associated gamma interferon. On the other hand, the liposomes may contribute in other ways to improving the therapeutic potential of gamma interferon. |
Hume, D. A.; Denkins, Y. M. Activation of macrophages to express cytocidal activity correlates with inhibition of their responsiveness to macrophage colony-stimulating factor (CSF-1): involvement of a pertussis toxin-sensitive reaction (Journal Article) In: Immunology and Cell Biology, vol. 67, no. 4, pp. 243–249, 1989, ISSN: 08189641. @article{hume_activation_1989,
title = {Activation of macrophages to express cytocidal activity correlates with inhibition of their responsiveness to macrophage colony-stimulating factor (CSF-1): involvement of a pertussis toxin-sensitive reaction},
author = {D. A. Hume and Y. M. Denkins},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0024324199&doi=10.1038%2ficb.1989.37&partnerID=40&md5=4998b8dbbcff00196ac74a8f47379e14},
doi = {10.1038/icb.1989.37},
issn = {08189641},
year = {1989},
date = {1989-01-01},
journal = {Immunology and Cell Biology},
volume = {67},
number = {4},
pages = {243--249},
abstract = {Bone marrow-derived murine macrophages were used to study the relationship between the proliferative response of macrophages to macrophage colony-stimulating factor (CSF-1) and their activation for cytocidal activity against tumour cells. Macrophage activation required two sequential signals. Lymphokines (gamma interferon, interleukin-4) provided the first (priming) signal; bacterial products (lipopolysaccharide, lipophilic muramyl tripeptide, lipopeptide 31362, pertussis toxin) provided the second (triggering) signal. Both priming and triggering agents inhibited [3H]-thymidine uptake by macrophages stimulated with CSF-1. The antiproliferative activity of priming and triggering stimuli was synergistic. Pretreatment with triggering stimuli at 37°C caused a rapid reduction of the subsequent binding of [125I]-CSF-1 to the cell surface at 4°C, whereas priming agents had relatively little effect. Growth inhibition by both priming and triggering agents was largely reversible by washing the cells, and occurred even when they were added as long as 24 h after the growth factor. The ability of pertussis toxin to both inhibit CSF-1-induced proliferation and trigger cytotoxicity in macrophages suggests the involvement of a regulatory GTP-binding protein (G protein) in both processes.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Bone marrow-derived murine macrophages were used to study the relationship between the proliferative response of macrophages to macrophage colony-stimulating factor (CSF-1) and their activation for cytocidal activity against tumour cells. Macrophage activation required two sequential signals. Lymphokines (gamma interferon, interleukin-4) provided the first (priming) signal; bacterial products (lipopolysaccharide, lipophilic muramyl tripeptide, lipopeptide 31362, pertussis toxin) provided the second (triggering) signal. Both priming and triggering agents inhibited [3H]-thymidine uptake by macrophages stimulated with CSF-1. The antiproliferative activity of priming and triggering stimuli was synergistic. Pretreatment with triggering stimuli at 37°C caused a rapid reduction of the subsequent binding of [125I]-CSF-1 to the cell surface at 4°C, whereas priming agents had relatively little effect. Growth inhibition by both priming and triggering agents was largely reversible by washing the cells, and occurred even when they were added as long as 24 h after the growth factor. The ability of pertussis toxin to both inhibit CSF-1-induced proliferation and trigger cytotoxicity in macrophages suggests the involvement of a regulatory GTP-binding protein (G protein) in both processes. |
1988
|
Schackert, G.; Simmons, R. D.; Buzbee, T. M.; Hume, D. A.; Fidler, I. J. Macrophage infiltration into experimental brain metastases: Occurrence through an intact blood-brain barrier (Journal Article) In: Journal of the National Cancer Institute, vol. 80, no. 13, pp. 1027–1034, 1988, ISSN: 00278874. @article{schackert_macrophage_1988,
title = {Macrophage infiltration into experimental brain metastases: Occurrence through an intact blood-brain barrier},
author = {G. Schackert and R. D. Simmons and T. M. Buzbee and D. A. Hume and I. J. Fidler},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023684344&doi=10.1093%2fjnci%2f80.13.1027&partnerID=40&md5=b413f5b9da3f4908dbcc65738488661e},
doi = {10.1093/jnci/80.13.1027},
issn = {00278874},
year = {1988},
date = {1988-01-01},
journal = {Journal of the National Cancer Institute},
volume = {80},
number = {13},
pages = {1027--1034},
abstract = {The purpose of this study was to examine the nature of the bllod-brain barrier in experimental brain metastases. Syngeneic fibrosarcoma or melanoma cells were injected into the internal carotid arteries of mice. Several weeks later, once the experimental brain metastases were established, the mice were given injections iv of sodium fluorescein.The capillaries within the metastatic foci were enlarged and irregular, but there was no leakage of sodium fluorescein, showing that the blood-brain barrier was intact. The neoplastic lesions were infiltrated by mononuclear phagocytes, which were identified by immunohistochemical localization of the macrophage-specific antigen F4/80, class II major histocom-patibility complex (MHC) antigens, and the macrophage product interleukin-1(IL-1). The metastatic foci contained numerous stellate macrophages that expressed F4/80 and MHC class II antigens, but little IL-1. Round, Monocyte-like F4/80 and MHC class II-positive cells were also observed within the tumor lesions and adhering to walls of the tumor microvasculature. Mice with fibrosarcoma brain metastases also had edematous lesions at sites remote from the metastatic foci that contained numerous astrocytes expressing class II MHC but not F4/80 antigens. In conclusion, the blood-brain barrier is intact within experimental brain metastases, yet macrophages of blood monocyte origin can infiltrage the lesions. [J Natl Cancer Inst 1988;80:1027-1034]. © 1988 Oxford University Press.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The purpose of this study was to examine the nature of the bllod-brain barrier in experimental brain metastases. Syngeneic fibrosarcoma or melanoma cells were injected into the internal carotid arteries of mice. Several weeks later, once the experimental brain metastases were established, the mice were given injections iv of sodium fluorescein.The capillaries within the metastatic foci were enlarged and irregular, but there was no leakage of sodium fluorescein, showing that the blood-brain barrier was intact. The neoplastic lesions were infiltrated by mononuclear phagocytes, which were identified by immunohistochemical localization of the macrophage-specific antigen F4/80, class II major histocom-patibility complex (MHC) antigens, and the macrophage product interleukin-1(IL-1). The metastatic foci contained numerous stellate macrophages that expressed F4/80 and MHC class II antigens, but little IL-1. Round, Monocyte-like F4/80 and MHC class II-positive cells were also observed within the tumor lesions and adhering to walls of the tumor microvasculature. Mice with fibrosarcoma brain metastases also had edematous lesions at sites remote from the metastatic foci that contained numerous astrocytes expressing class II MHC but not F4/80 antigens. In conclusion, the blood-brain barrier is intact within experimental brain metastases, yet macrophages of blood monocyte origin can infiltrage the lesions. [J Natl Cancer Inst 1988;80:1027-1034]. © 1988 Oxford University Press. |
McLachlan, J. C.; Macintyre, J.; Hume, D. D.; Smith, J. Direct demonstration of production of transforming growth factor activity by embryonic chick tissue (Journal Article) In: Experientia, vol. 44, no. 4, pp. 351–352, 1988, ISSN: 00144754, (Publisher: Birkhäuser-Verlag). @article{mclachlan_direct_1988,
title = {Direct demonstration of production of transforming growth factor activity by embryonic chick tissue},
author = {J. C. McLachlan and J. Macintyre and D. D. Hume and J. Smith},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023877161&doi=10.1007%2fBF01961280&partnerID=40&md5=e9f73455c8530a92bd7bb879b1a2d4d2},
doi = {10.1007/BF01961280},
issn = {00144754},
year = {1988},
date = {1988-01-01},
journal = {Experientia},
volume = {44},
number = {4},
pages = {351--352},
abstract = {The presence of transforming growth factor activity in early chick embryos was directly demonstrated by the ability of limb and tail buds to induce anchorage independent division in NRK 49f cells. Colony number increased with limb bud number and developmental stage. Medium conditioned by tail buds contained some stimulating effect, and strongly promoted the action of other transforming growth factors. © 1988 Birkhäuser Verlag.},
note = {Publisher: Birkhäuser-Verlag},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The presence of transforming growth factor activity in early chick embryos was directly demonstrated by the ability of limb and tail buds to induce anchorage independent division in NRK 49f cells. Colony number increased with limb bud number and developmental stage. Medium conditioned by tail buds contained some stimulating effect, and strongly promoted the action of other transforming growth factors. © 1988 Birkhäuser Verlag. |
Russell, P. J.; Philips, J.; Allan, W.; Hume, D. A. Antigenic variation and macrophage infiltration of human bladder tumors xenografted into nude mice (Journal Article) In: Journal of Leukocyte Biology, vol. 43, no. 4, pp. 335–342, 1988, ISSN: 07415400. @article{russell_antigenic_1988,
title = {Antigenic variation and macrophage infiltration of human bladder tumors xenografted into nude mice},
author = {P. J. Russell and J. Philips and W. Allan and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023915244&doi=10.1002%2fjlb.43.4.335&partnerID=40&md5=ce22a1468c2e7c02344b68147569cbbb},
doi = {10.1002/jlb.43.4.335},
issn = {07415400},
year = {1988},
date = {1988-01-01},
journal = {Journal of Leukocyte Biology},
volume = {43},
number = {4},
pages = {335--342},
abstract = {The presence of macrophages both within and aroung human bladder transitional cell carcinomas xenografted into nude mice has been examined using immunocytochemical staining. Nine different xenograft lines derived from bladder tumors of eight patients were stained for F4/80, MHC II and PGP-1 labelled cells. The results revealed considerable heterogeneity both within and between tumors. All of the tumors generated some macrophage response at the tumor periphery, and this was marked in two instances, UCRU-BL-13, passage 9 and UCRU-BL-17, passage 2. In only two tumors was there substantial penetration of the tumor epithelium by macrophages, though infiltrating Ia+, F4/80+, PGP-1+ cells were sometimes seen spreading along the base of the epithelial sheets. Three of the tumors were characterized by the presence of L3T4+ T lymphocytes at the invasion front. The presence of macrophages or lymphocytes either at the invasion front or within the tumors did not correlate with the pathological grade of the tumors. PGP-1 monoclonal antibodies also stained granulocytes, which were present within the tumor mass in UCRU-BL-15, passage 2, possibly reflecting the production by the tumor of G-CSF. In addition, the PGP-1 antibodies stained some of the bladder tumor cells themselves, and, in some cases, the interstitial structures within the tumors. The significance of this staining is not yet understood. The xenografted tumors will provide a useful model to examine the constraints on tumor therapy using macrophage activating stimuli.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The presence of macrophages both within and aroung human bladder transitional cell carcinomas xenografted into nude mice has been examined using immunocytochemical staining. Nine different xenograft lines derived from bladder tumors of eight patients were stained for F4/80, MHC II and PGP-1 labelled cells. The results revealed considerable heterogeneity both within and between tumors. All of the tumors generated some macrophage response at the tumor periphery, and this was marked in two instances, UCRU-BL-13, passage 9 and UCRU-BL-17, passage 2. In only two tumors was there substantial penetration of the tumor epithelium by macrophages, though infiltrating Ia+, F4/80+, PGP-1+ cells were sometimes seen spreading along the base of the epithelial sheets. Three of the tumors were characterized by the presence of L3T4+ T lymphocytes at the invasion front. The presence of macrophages or lymphocytes either at the invasion front or within the tumors did not correlate with the pathological grade of the tumors. PGP-1 monoclonal antibodies also stained granulocytes, which were present within the tumor mass in UCRU-BL-15, passage 2, possibly reflecting the production by the tumor of G-CSF. In addition, the PGP-1 antibodies stained some of the bladder tumor cells themselves, and, in some cases, the interstitial structures within the tumors. The significance of this staining is not yet understood. The xenografted tumors will provide a useful model to examine the constraints on tumor therapy using macrophage activating stimuli. |
Simeonovic, C. J.; Hodder, M. J.; Hume, D. A. Role of Ia-positive leukocytes and F4/80-positive macrophages in the immunogenicity of fetal mouse proislets and fetal pancreas (Journal Article) In: Transplantation Proceedings, vol. 20, no. 1, pp. 68–71, 1988, ISSN: 00411345. @article{simeonovic_role_1988,
title = {Role of Ia-positive leukocytes and F4/80-positive macrophages in the immunogenicity of fetal mouse proislets and fetal pancreas},
author = {C. J. Simeonovic and M. J. Hodder and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023830008&partnerID=40&md5=c4e5e6fb1230f604c856da9249846453},
issn = {00411345},
year = {1988},
date = {1988-01-01},
journal = {Transplantation Proceedings},
volume = {20},
number = {1},
pages = {68--71},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Hume, D. A.; Pavli, P.; Donahue, R. E.; Fidler, I. J. The effect of human recombinant macrophage colony-stimulating factor (CSF-1) on the murine mononuclear phagocyte system in vivo (Journal Article) In: Journal of Immunology, vol. 141, no. 10, pp. 3405–3409, 1988, ISSN: 00221767. @article{hume_effect_1988,
title = {The effect of human recombinant macrophage colony-stimulating factor (CSF-1) on the murine mononuclear phagocyte system in vivo},
author = {D. A. Hume and P. Pavli and R. E. Donahue and I. J. Fidler},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023685533&partnerID=40&md5=21bc3cdd61c1e8d1f6db783ae3e170ff},
issn = {00221767},
year = {1988},
date = {1988-01-01},
journal = {Journal of Immunology},
volume = {141},
number = {10},
pages = {3405--3409},
abstract = {Human recombinant macrophage CSF (CSF-1) was administered i.v. to mice. After four daily injections there was a dose-dependent increase in the responsiveness of bone marrow cells from the treated animals to CSF-1 in vitro. At the highest dose tested (20,000 U/day) there was a selective 10-fold increase in the circulating population of mature monocytes. CSF-1 treatment also increased the macrophage content of the liver and peritoneal cavity and caused splenomegaly. The macrophages isolated from the peritoneum of CSF-1-treated animals were larger and expressed higher levels of the macrophage-specific F4/80 Ag. These data demonstrate that CSF-1 can act as a circulating regulator of the mononuclear phagocyte system.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Human recombinant macrophage CSF (CSF-1) was administered i.v. to mice. After four daily injections there was a dose-dependent increase in the responsiveness of bone marrow cells from the treated animals to CSF-1 in vitro. At the highest dose tested (20,000 U/day) there was a selective 10-fold increase in the circulating population of mature monocytes. CSF-1 treatment also increased the macrophage content of the liver and peritoneal cavity and caused splenomegaly. The macrophages isolated from the peritoneum of CSF-1-treated animals were larger and expressed higher levels of the macrophage-specific F4/80 Ag. These data demonstrate that CSF-1 can act as a circulating regulator of the mononuclear phagocyte system. |
1987
|
Hume, D. A. Growth regulation in murine bone marrow-derived macrophages: Effects of contaminating endotoxin in commercial GM CSF and interleukin 4 (Journal Article) In: Lymphokine Research, vol. 6, no. 4, pp. 357–359, 1987, ISSN: 02776766. @article{hume_growth_1987,
title = {Growth regulation in murine bone marrow-derived macrophages: Effects of contaminating endotoxin in commercial GM CSF and interleukin 4},
author = {D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023609509&partnerID=40&md5=7fd6fa37f52e0c8902fd655777345b5f},
issn = {02776766},
year = {1987},
date = {1987-01-01},
journal = {Lymphokine Research},
volume = {6},
number = {4},
pages = {357--359},
abstract = {Murine bone marrow-derived macrophages have been used extensively in studies of the action of macrophage colony-stimulating factor (CSF-1), which is required for their survival and proliferation (1,2). In the course of such studies it has become clear that agents which stimulate macrophage cytocidal activity oppose the induction of proliferation in response to CSF-1 (2). Two recent additions to the family of proposed macrophage activators are granulocyte-macrophage colony stimulating factor (GM-CSF,3,4) and B-cell stimulating factor (IL-4,4,5). Genes encoding both of these factors have been isolated and recombinant molecules are available commercially. I therefore purchased aliquots of GM-CSF and IL-4 from Genzyme (Cambridge, Mass) and studied their activity on the proliferation of bone marrow-derived macrophages.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Murine bone marrow-derived macrophages have been used extensively in studies of the action of macrophage colony-stimulating factor (CSF-1), which is required for their survival and proliferation (1,2). In the course of such studies it has become clear that agents which stimulate macrophage cytocidal activity oppose the induction of proliferation in response to CSF-1 (2). Two recent additions to the family of proposed macrophage activators are granulocyte-macrophage colony stimulating factor (GM-CSF,3,4) and B-cell stimulating factor (IL-4,4,5). Genes encoding both of these factors have been isolated and recombinant molecules are available commercially. I therefore purchased aliquots of GM-CSF and IL-4 from Genzyme (Cambridge, Mass) and studied their activity on the proliferation of bone marrow-derived macrophages. |
Hume, D. A.; Allan, W.; Fabrus, B.; Weidemann, M. J.; Hapel, A. J.; Bartelmez, S. Regulation of proliferation of bone marrow-derived macrophages (Journal Article) In: Lymphokine Research, vol. 6, no. 2, pp. 127–139, 1987, ISSN: 02776766. @article{hume_regulation_1987,
title = {Regulation of proliferation of bone marrow-derived macrophages},
author = {D. A. Hume and W. Allan and B. Fabrus and M. J. Weidemann and A. J. Hapel and S. Bartelmez},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023259007&partnerID=40&md5=06f6b636793d1b61e3e325ca04933a7d},
issn = {02776766},
year = {1987},
date = {1987-01-01},
journal = {Lymphokine Research},
volume = {6},
number = {2},
pages = {127--139},
abstract = {The rate of mobilisation of macrophages from marrow is an important determinant of the outcome of many pathological lesions. Studies of BMDM have provided insight into the complex feedback regulation that may control macrophage production. In addition BMDM possess several properties in common with transformed cells of other tissue origins and an understanding of their growth regulation may provide an insight into the mechanism of malignant transformation.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The rate of mobilisation of macrophages from marrow is an important determinant of the outcome of many pathological lesions. Studies of BMDM have provided insight into the complex feedback regulation that may control macrophage production. In addition BMDM possess several properties in common with transformed cells of other tissue origins and an understanding of their growth regulation may provide an insight into the mechanism of malignant transformation. |
Müllbacher, A.; Hume, D.; Braithwaite, A. W.; Waring, P.; Eichner, R. D. Selective resistance of bone marrow-derived hemopoietic progenitor cells to gliotoxin (Journal Article) In: Proceedings of the National Academy of Sciences of the United States of America, vol. 84, no. 11, pp. 3822–3825, 1987, ISSN: 00278424. @article{mullbacher_selective_1987,
title = {Selective resistance of bone marrow-derived hemopoietic progenitor cells to gliotoxin},
author = {A. Müllbacher and D. Hume and A. W. Braithwaite and P. Waring and R. D. Eichner},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023225941&doi=10.1073%2fpnas.84.11.3822&partnerID=40&md5=37c0ecd23c3da2572956d031292511ce},
doi = {10.1073/pnas.84.11.3822},
issn = {00278424},
year = {1987},
date = {1987-01-01},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {84},
number = {11},
pages = {3822--3825},
abstract = {The fungal metabolite gliotoxin at low concentrations prevents mitogen stimulation of mature lymphocytes as a result of gliotoxin-induced genomic DNA degradation. Bone marrow, on the other hand, contains a subpopulation of cells resistant to gliotoxin at similar concentrations. This population includes the hemopoietic progenitor cells that grow in vitro in response to appropriate colony-stimulating factors and cells that form colonies in the spleens of lethally irradiated recipients. Gliotoxin treatment of lymph node cell-enriched bone marrow significantly delayed the onset of graft-versus-host disease in fully allogeneic bone marrow chimeras.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The fungal metabolite gliotoxin at low concentrations prevents mitogen stimulation of mature lymphocytes as a result of gliotoxin-induced genomic DNA degradation. Bone marrow, on the other hand, contains a subpopulation of cells resistant to gliotoxin at similar concentrations. This population includes the hemopoietic progenitor cells that grow in vitro in response to appropriate colony-stimulating factors and cells that form colonies in the spleens of lethally irradiated recipients. Gliotoxin treatment of lymph node cell-enriched bone marrow significantly delayed the onset of graft-versus-host disease in fully allogeneic bone marrow chimeras. |
Hume, D. A.; Allan, W.; Hogan, P. G.; Doe, W. F. Immunohistochemical characterisation of macrophages in human liver and gastrointestinal tract: Expression of CD4, HLA-DR, OKM1, and the mature macrophage marker 25F9 in normal and diseased tissue (Journal Article) In: Journal of Leukocyte Biology, vol. 42, no. 5, pp. 474–484, 1987, ISSN: 07415400. @article{hume_immunohistochemical_1987,
title = {Immunohistochemical characterisation of macrophages in human liver and gastrointestinal tract: Expression of CD4, HLA-DR, OKM1, and the mature macrophage marker 25F9 in normal and diseased tissue},
author = {D. A. Hume and W. Allan and P. G. Hogan and W. F. Doe},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023636846&doi=10.1002%2fjlb.42.5.474&partnerID=40&md5=9feb25d92a5e0e6afcacee927582541f},
doi = {10.1002/jlb.42.5.474},
issn = {07415400},
year = {1987},
date = {1987-01-01},
journal = {Journal of Leukocyte Biology},
volume = {42},
number = {5},
pages = {474--484},
abstract = {This report describes the immunocytochemical characterisation of macrophages in sections of human liver, gastrointestinal tract, and associated lymphoid tissue and the inflammatory lesions of Crohn's disease. 25F9 is an antigen reported to be induced during the maturation of blood monocytes in vitro. The antigen was concentrated in cytoplasmic vesicular structures of isolated gastrointestinal macrophages. Similar labelled cells were observed in the apical regions of lamina propria in both small and large intestine in vivo. Their numbers and size were greatly increased in specimens of colon from patients with melanosis coli. Mucosal inflammatory lesions in specimens from patients with Crohn's disease did not contain 25F9-positive cells. The antigen was absent from giant cells and epithelioid cells in granulomata but was expressed on histiocytes in submucosal microgranulomata. In lymphoid organs, 25F9-positive cells were found in germinal centres, in the dome region of Peyer's patch, and in the medulla, but were largely excluded from T cell areas. In reactive nodes from Crohn's disease patients, the number of labelled cells in germinal centres and T cell areas was greatly increased. 25F9 was absent from the majority of typical liver Kupffer cells, but was expressed on cytoplasmic granules in a minor subpopulation of larger, more rounded cells in the liver. The results suggest that 25F9 is a marker for endocytosis rather than maturation. In parallel sections, resident macrophages of both liver and gastrointestinal tract labelled with Leu 3a/OKT4 (CD4) and with OKIa (HLA-DR antigen) but did not express OKM1 (type III complement receptor). By contrast, OKM1 was present on inflammatory cells, epithelioid cells, and giant cells in mucosal lesions of Crohn's disease.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
This report describes the immunocytochemical characterisation of macrophages in sections of human liver, gastrointestinal tract, and associated lymphoid tissue and the inflammatory lesions of Crohn's disease. 25F9 is an antigen reported to be induced during the maturation of blood monocytes in vitro. The antigen was concentrated in cytoplasmic vesicular structures of isolated gastrointestinal macrophages. Similar labelled cells were observed in the apical regions of lamina propria in both small and large intestine in vivo. Their numbers and size were greatly increased in specimens of colon from patients with melanosis coli. Mucosal inflammatory lesions in specimens from patients with Crohn's disease did not contain 25F9-positive cells. The antigen was absent from giant cells and epithelioid cells in granulomata but was expressed on histiocytes in submucosal microgranulomata. In lymphoid organs, 25F9-positive cells were found in germinal centres, in the dome region of Peyer's patch, and in the medulla, but were largely excluded from T cell areas. In reactive nodes from Crohn's disease patients, the number of labelled cells in germinal centres and T cell areas was greatly increased. 25F9 was absent from the majority of typical liver Kupffer cells, but was expressed on cytoplasmic granules in a minor subpopulation of larger, more rounded cells in the liver. The results suggest that 25F9 is a marker for endocytosis rather than maturation. In parallel sections, resident macrophages of both liver and gastrointestinal tract labelled with Leu 3a/OKT4 (CD4) and with OKIa (HLA-DR antigen) but did not express OKM1 (type III complement receptor). By contrast, OKM1 was present on inflammatory cells, epithelioid cells, and giant cells in mucosal lesions of Crohn's disease. |
Warren, H. S.; Simeonovic, C. J.; Allan, W.; Hume, D. A. Induced expression of class II major histocompatibility complex antigens on thyroid but not pancreatic islet allografts following transfer of sensitized LYT2+ Ŧ cells (Journal Article) In: Transplantation Proceedings, vol. 19, no. 1 I, pp. 213, 1987, ISSN: 00411345. @article{warren_induced_1987,
title = {Induced expression of class II major histocompatibility complex antigens on thyroid but not pancreatic islet allografts following transfer of sensitized LYT2+ Ŧ cells},
author = {H. S. Warren and C. J. Simeonovic and W. Allan and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023117043&partnerID=40&md5=590e1202e54dd88eaa83a6014d6107f6},
issn = {00411345},
year = {1987},
date = {1987-01-01},
journal = {Transplantation Proceedings},
volume = {19},
number = {1 I},
pages = {213},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
1986
|
Dixon, J. E.; Allan, J. E.; Doherty, P. C.; Hume, D. A. Immunohistochemical analysis of the involvement of F4/80 and Ia-positive macrophages in mouse liver infected with lymphocytic choriomeningitis virus (Journal Article) In: Journal of Leukocyte Biology, vol. 40, no. 5, pp. 617–628, 1986, ISSN: 07415400. @article{dixon_immunohistochemical_1986,
title = {Immunohistochemical analysis of the involvement of F4/80 and Ia-positive macrophages in mouse liver infected with lymphocytic choriomeningitis virus},
author = {J. E. Dixon and J. E. Allan and P. C. Doherty and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0022526865&doi=10.1002%2fjlb.40.5.617&partnerID=40&md5=7e85007a54f6b8a2c585970a896f4339},
doi = {10.1002/jlb.40.5.617},
issn = {07415400},
year = {1986},
date = {1986-01-01},
journal = {Journal of Leukocyte Biology},
volume = {40},
number = {5},
pages = {617--628},
abstract = {The distribution of cells bearing the F4/80 macrophage marker and class II MHC glycoproteins has been analyzed in the livers of mice infected with viscerotropic LCMV. The number of F4/80+ macrophages in the liver increases greatly during infection. Much of this is due to the localization of F4/80+ Ia+ monocytes, large numbers of which attach to the walls of the sinuses and the central and hepatic veins. Numerous lymphocytes are also observed in the sinusoids, frequently in close association with macrophages. The lymphocytes tend to move on from this intravascular location, while the macrophages remain. Foci of F4/80- Ia- mononuclear cells (probably T lymphocytes) are found both in the liver parenchyma and in locations that are obviously perivascular. The most prominent of these lymphocyte cuffs are located in the region of the portal triad. Infiltration of the lymphocyte foci with F4/80+ Ia+ elements occurs late, concurrent with evidence of cell death within the lesion. The dissociation in the focal accumulations of lymphocytes and monocyte/macrophages early in the disease process is both striking and unforeseen.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The distribution of cells bearing the F4/80 macrophage marker and class II MHC glycoproteins has been analyzed in the livers of mice infected with viscerotropic LCMV. The number of F4/80+ macrophages in the liver increases greatly during infection. Much of this is due to the localization of F4/80+ Ia+ monocytes, large numbers of which attach to the walls of the sinuses and the central and hepatic veins. Numerous lymphocytes are also observed in the sinusoids, frequently in close association with macrophages. The lymphocytes tend to move on from this intravascular location, while the macrophages remain. Foci of F4/80- Ia- mononuclear cells (probably T lymphocytes) are found both in the liver parenchyma and in locations that are obviously perivascular. The most prominent of these lymphocyte cuffs are located in the region of the portal triad. Infiltration of the lymphocyte foci with F4/80+ Ia+ elements occurs late, concurrent with evidence of cell death within the lesion. The dissociation in the focal accumulations of lymphocytes and monocyte/macrophages early in the disease process is both striking and unforeseen. |
Gordon, S.; Crocker, P. R.; Morris, L.; Lee, S. H.; Perry, V. H.; Hume, D. A. Localization and function of tissue macrophages. (Journal Article) In: Ciba Foundation symposium, vol. 118, pp. 54–67, 1986, ISSN: 03005208. @article{gordon_localization_1986,
title = {Localization and function of tissue macrophages.},
author = {S. Gordon and P. R. Crocker and L. Morris and S. H. Lee and V. H. Perry and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0022438725&partnerID=40&md5=c0d31816497f174684a6a800a17d8170},
issn = {03005208},
year = {1986},
date = {1986-01-01},
journal = {Ciba Foundation symposium},
volume = {118},
pages = {54--67},
abstract = {The rat monoclonal antibody F4/80 defines a plasma membrane glycoprotein of about 160 kilodaltons that is expressed by mature mouse macrophages. The antigen has been used to define macrophage distribution within the mouse (normal adult, embryo, infection models) by cytochemistry and quantitative immunochemical analysis. Macrophages migrate into fetal and adult haemopoietic and other tissues in an ordered sequence. The surface properties of 'fixed' macrophages isolated from various organs (bone marrow, liver, spleen) are distinct from those of circulating monocytes or free cells (peritoneal and pleural cavities, alveolar) and may play a role in local adhesion and trophic interactions with other cells.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The rat monoclonal antibody F4/80 defines a plasma membrane glycoprotein of about 160 kilodaltons that is expressed by mature mouse macrophages. The antigen has been used to define macrophage distribution within the mouse (normal adult, embryo, infection models) by cytochemistry and quantitative immunochemical analysis. Macrophages migrate into fetal and adult haemopoietic and other tissues in an ordered sequence. The surface properties of 'fixed' macrophages isolated from various organs (bone marrow, liver, spleen) are distinct from those of circulating monocytes or free cells (peritoneal and pleural cavities, alveolar) and may play a role in local adhesion and trophic interactions with other cells. |
1985
|
Hume, D. A. The biology of macrophages. (Journal Article) In: Science progress, vol. 69, no. 276, pp. 485–494, 1985, ISSN: 00368504. @article{hume_biology_1985,
title = {The biology of macrophages.},
author = {D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0022325981&partnerID=40&md5=d10b7ef72f243eeba0d668d3db42aad8},
issn = {00368504},
year = {1985},
date = {1985-01-01},
journal = {Science progress},
volume = {69},
number = {276},
pages = {485--494},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Hapel, A. J.; Osborne, J. M.; Fung, O. M.; Young, I. G.; Allan, W.; Hume, D. A. Expression of 20-α-hydroxysteroid dehydrogenase in mouse macrophages, hemopoietic cells, and cell lines and its induction by colony-stimulating factors (Journal Article) In: Journal of Immunology, vol. 134, no. 4, pp. 2492–2497, 1985, ISSN: 00221767. @article{hapel_expression_1985,
title = {Expression of 20-α-hydroxysteroid dehydrogenase in mouse macrophages, hemopoietic cells, and cell lines and its induction by colony-stimulating factors},
author = {A. J. Hapel and J. M. Osborne and O. M. Fung and I. G. Young and W. Allan and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021925593&partnerID=40&md5=320d7bb6551ce2b8af8afdb9ed018733},
issn = {00221767},
year = {1985},
date = {1985-01-01},
journal = {Journal of Immunology},
volume = {134},
number = {4},
pages = {2492--2497},
abstract = {The enzyme 20-α-hydroxysteroid dehydrogenase (20αSDH) has been proposed as a T lymphocyte marker that is specifically induced by interleukin 3. We have examined the expression of 20αSDH and its relationship to interleukin 3 responsiveness in other hemopoietic lineages. The enzyme is expressed at high levels in the bone marrow of athymic nu/nu mice, but only at low levels in nu/nu spleen and normal adult bone marrow. 20αSDH is induced in nu/nu spleen and in normal fetal liver cells by granulocyte-macrophage colony-stimulating factor (GM-CSF) as well as by interleukin 3. In longer term cultures of fetal liver and adult marrow, macrophage colony-stimulating factor (M-CSF) also induces the enzyme, which is expressed in proliferating adherent macrophages. The high levels of 20αSDH in purified bone marrow-derived macrophages are maintained by M-CSF, GM-CSF, or interleukin 3. Expression of 20αSDH in these cells is associated with resistance to growth inhibition by progesterone. Additional evidence against the restriction of 20αSDH to T lymphocytes is found in its presence in peritoneal macrophages, myelomonocytic and macrophage-like cell lines, and the L929 fibrosarcoma line. We conclude that 20αSDH is a normal enzyme of proliferating hemopoietic cells irrespective of their lineage or growth factor responsiveness.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The enzyme 20-α-hydroxysteroid dehydrogenase (20αSDH) has been proposed as a T lymphocyte marker that is specifically induced by interleukin 3. We have examined the expression of 20αSDH and its relationship to interleukin 3 responsiveness in other hemopoietic lineages. The enzyme is expressed at high levels in the bone marrow of athymic nu/nu mice, but only at low levels in nu/nu spleen and normal adult bone marrow. 20αSDH is induced in nu/nu spleen and in normal fetal liver cells by granulocyte-macrophage colony-stimulating factor (GM-CSF) as well as by interleukin 3. In longer term cultures of fetal liver and adult marrow, macrophage colony-stimulating factor (M-CSF) also induces the enzyme, which is expressed in proliferating adherent macrophages. The high levels of 20αSDH in purified bone marrow-derived macrophages are maintained by M-CSF, GM-CSF, or interleukin 3. Expression of 20αSDH in these cells is associated with resistance to growth inhibition by progesterone. Additional evidence against the restriction of 20αSDH to T lymphocytes is found in its presence in peritoneal macrophages, myelomonocytic and macrophage-like cell lines, and the L929 fibrosarcoma line. We conclude that 20αSDH is a normal enzyme of proliferating hemopoietic cells irrespective of their lineage or growth factor responsiveness. |
Hume, D. A.; Summers, K. M.; Cohen, D. R.; Allan, W. Regulation of the production of granulocyte-macrophage colony-stimulating factor by macrophage-like tumour cell lines (Journal Article) In: FEBS Letters, vol. 180, no. 2, pp. 271–274, 1985, ISSN: 00145793. @article{hume_regulation_1985,
title = {Regulation of the production of granulocyte-macrophage colony-stimulating factor by macrophage-like tumour cell lines},
author = {D. A. Hume and K. M. Summers and D. R. Cohen and W. Allan},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021930197&doi=10.1016%2f0014-5793%2885%2981084-X&partnerID=40&md5=73f20ae9954007c7a9d745bd8dde27c6},
doi = {10.1016/0014-5793(85)81084-X},
issn = {00145793},
year = {1985},
date = {1985-01-01},
journal = {FEBS Letters},
volume = {180},
number = {2},
pages = {271--274},
abstract = {Macrophage tumour cell lines (PU5-1.8, P388D1) produced detectable granulocyte macrophage colonystimulating (CSF-2) activity measured using a factor-dependent cell line FDC-P1. The production ofCSF-2 was enhanced by endotoxin and inhibited by serum, and correlated inversely with [3H]TdR incorporation. mRNA isolated from PU5-1.8 or P388D1 cells initiated CSF-2 production when injected into Xenopus laevis oocytes. The specific activity in this assay was unaltered in mRNA isolated from endotoxin-treated cells. The results suggest that endotoxin acts at a post-transcriptional level. © 1985.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Macrophage tumour cell lines (PU5-1.8, P388D1) produced detectable granulocyte macrophage colonystimulating (CSF-2) activity measured using a factor-dependent cell line FDC-P1. The production ofCSF-2 was enhanced by endotoxin and inhibited by serum, and correlated inversely with [3H]TdR incorporation. mRNA isolated from PU5-1.8 or P388D1 cells initiated CSF-2 production when injected into Xenopus laevis oocytes. The specific activity in this assay was unaltered in mRNA isolated from endotoxin-treated cells. The results suggest that endotoxin acts at a post-transcriptional level. © 1985. |
Perry, V. H.; Hume, D. A.; Gordon, S. Immunohistochemical localization of macrophages and microglia in the adult and developing mouse brain (Journal Article) In: Neuroscience, vol. 15, no. 2, pp. 313–326, 1985, ISSN: 03064522. @article{perry_immunohistochemical_1985,
title = {Immunohistochemical localization of macrophages and microglia in the adult and developing mouse brain},
author = {V. H. Perry and D. A. Hume and S. Gordon},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0022387412&doi=10.1016%2f0306-4522%2885%2990215-5&partnerID=40&md5=33ca6ecbb2979792b24bda31e1524c37},
doi = {10.1016/0306-4522(85)90215-5},
issn = {03064522},
year = {1985},
date = {1985-01-01},
journal = {Neuroscience},
volume = {15},
number = {2},
pages = {313--326},
abstract = {Macrophages and microglia in the developing and adult mouse brain have been identified by is consistent with the idea that dying neurons and axons provide a stimulus for macrophage infiltration. Our results provide strong support for the hypothesis that the microglia are derived from monocytes and show that microglia possess receptors which would allow them to play a part in the immune defence of the nervous system. © 1985.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Macrophages and microglia in the developing and adult mouse brain have been identified by is consistent with the idea that dying neurons and axons provide a stimulus for macrophage infiltration. Our results provide strong support for the hypothesis that the microglia are derived from monocytes and show that microglia possess receptors which would allow them to play a part in the immune defence of the nervous system. © 1985. |
Hume, D. A. Immunohistochemical Analysis of Murine Mononuclear Phagocytes that Express Class II Major Histocompatibility Antigens (Journal Article) In: Immunobiology, vol. 170, no. 5, pp. 381–389, 1985, ISSN: 01712985. @article{hume_immunohistochemical_1985,
title = {Immunohistochemical Analysis of Murine Mononuclear Phagocytes that Express Class II Major Histocompatibility Antigens},
author = {D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0022378130&doi=10.1016%2fS0171-2985%2885%2980062-0&partnerID=40&md5=caf3fbdd0d9e899d493e46835a3bcf25},
doi = {10.1016/S0171-2985(85)80062-0},
issn = {01712985},
year = {1985},
date = {1985-01-01},
journal = {Immunobiology},
volume = {170},
number = {5},
pages = {381--389},
abstract = {Expression of class II major histocompatibility antigen(s) was analyzed in mouse tissue sections using an immunocytochemical techniqueParallel sections were stained for the macrophage-specific antigen F4/80MHCII antigen(s) were absent from the majority of F4/ 80+ cells in liver, bone marrow, splenic red pulp, and brain (microglia) but were present on intraepithelial, periepithelial, and free (e.galveolar) cells in gastrointestinal, urogenital, respiratory, and endocrine tissuesThe staining pattern in such tissues was not distinguishable from that of F4/80The results suggest that a major subpopulation of mononuclear phagocytes expresses MHCII antigen(s) constitutively. © 1985, Gustav Fischer Verlag · Stuttgart · New York. All rights reserved.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Expression of class II major histocompatibility antigen(s) was analyzed in mouse tissue sections using an immunocytochemical techniqueParallel sections were stained for the macrophage-specific antigen F4/80MHCII antigen(s) were absent from the majority of F4/ 80+ cells in liver, bone marrow, splenic red pulp, and brain (microglia) but were present on intraepithelial, periepithelial, and free (e.galveolar) cells in gastrointestinal, urogenital, respiratory, and endocrine tissuesThe staining pattern in such tissues was not distinguishable from that of F4/80The results suggest that a major subpopulation of mononuclear phagocytes expresses MHCII antigen(s) constitutively. © 1985, Gustav Fischer Verlag · Stuttgart · New York. All rights reserved. |
Hume, D. A.; Allan, W.; Golder, J.; Stephens, R. W.; Doe, W. F.; Warren, H. S. Preparation and characterization of human bone marrow-derived macrophages (Journal Article) In: Journal of Leukocyte Biology, vol. 38, no. 4, pp. 541–552, 1985, ISSN: 07415400. @article{hume_preparation_1985,
title = {Preparation and characterization of human bone marrow-derived macrophages},
author = {D. A. Hume and W. Allan and J. Golder and R. W. Stephens and W. F. Doe and H. S. Warren},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0022185367&doi=10.1002%2fjlb.38.4.541&partnerID=40&md5=950fbc90cd7002629b7231bfdf20f07a},
doi = {10.1002/jlb.38.4.541},
issn = {07415400},
year = {1985},
date = {1985-01-01},
journal = {Journal of Leukocyte Biology},
volume = {38},
number = {4},
pages = {541--552},
abstract = {Bone marrow-derived macrophages were prepared from human bone marrow mononuclear cells following cultivation in GCT-conditioned medium (GCT-CM) and purification by adherence to fibronectin-coated flasks. The growth of bone marrow mononuclear cells in GCT-CM was dependent on the shape of the culture vessels, being increased in round-bottomed versus flat-bottomed wells. Proliferation was confined to nonadherent cells; like blood monocytes, bone marrow-derived macrophages did not incorporate [3H]thymidine in response to GCT-CM or human serum. Purified macrophages from this source expressed nonspecific esterase and OKM1, OKIa, FMC 17, 32, and 34 and 25F9 antigens but lacked Mo2. They expressed high levels of an inactivator of plasminogen activator, minactivin, and gave a substantial metabolic burst in response to phorbol myristate acetate or opsonized (but not unopsonized) zymosan. Bone marrow-derived macrophages acted as accessory cells in the response of T lymphocytes to phytohemagglutinin. The results suggest that liquid bone marrow cultures are useful in the study of the differentiation of human mononuclear phagocytes.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Bone marrow-derived macrophages were prepared from human bone marrow mononuclear cells following cultivation in GCT-conditioned medium (GCT-CM) and purification by adherence to fibronectin-coated flasks. The growth of bone marrow mononuclear cells in GCT-CM was dependent on the shape of the culture vessels, being increased in round-bottomed versus flat-bottomed wells. Proliferation was confined to nonadherent cells; like blood monocytes, bone marrow-derived macrophages did not incorporate [3H]thymidine in response to GCT-CM or human serum. Purified macrophages from this source expressed nonspecific esterase and OKM1, OKIa, FMC 17, 32, and 34 and 25F9 antigens but lacked Mo2. They expressed high levels of an inactivator of plasminogen activator, minactivin, and gave a substantial metabolic burst in response to phorbol myristate acetate or opsonized (but not unopsonized) zymosan. Bone marrow-derived macrophages acted as accessory cells in the response of T lymphocytes to phytohemagglutinin. The results suggest that liquid bone marrow cultures are useful in the study of the differentiation of human mononuclear phagocytes. |
Russell, P. J.; Cahill, J.; Cameron, F.; Hume, D. Studies of peritoneal macrophage function in murine systemic lupus erythematosus. 2. Nature of elevated resident peritoneal cells in NZB and (NZB x NZW)F1 mice (Journal Article) In: Journal of Leukocyte Biology, vol. 38, no. 2, pp. 241–254, 1985, ISSN: 07415400. @article{russell_studies_1985,
title = {Studies of peritoneal macrophage function in murine systemic lupus erythematosus. 2. Nature of elevated resident peritoneal cells in NZB and (NZB x NZW)F1 mice},
author = {P. J. Russell and J. Cahill and F. Cameron and D. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021969157&doi=10.1002%2fjlb.38.2.241&partnerID=40&md5=6e899c08d465bc1a2a7b1fd51e807b12},
doi = {10.1002/jlb.38.2.241},
issn = {07415400},
year = {1985},
date = {1985-01-01},
journal = {Journal of Leukocyte Biology},
volume = {38},
number = {2},
pages = {241--254},
abstract = {The numbers of resident peritoneal cells recovered from NZB annd (NZB x NZW)F1 hybrid mice, which develop systemic lupus erythematosus (SLE), increased strikingly with age as compared with cells recovered from normal mice. The rise paralleled the onset of anti-DNA antibodies, occurring earlier in females than in males. The increased number of cells was due to an accumulation of medium-sized cells with an intermediate appearance, but with the functional characteristics and cell markers typical of a macrophage. The unusual cells were esterase, F4/80 and Mac-1 positive, peroxidase, and Alcian blue negative, and were shown on sedimentation velocity separation to be phagocytic for EA and C3 (serum-treated) zymosan; 47-48% of peritoneal cells were Ia positive.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The numbers of resident peritoneal cells recovered from NZB annd (NZB x NZW)F1 hybrid mice, which develop systemic lupus erythematosus (SLE), increased strikingly with age as compared with cells recovered from normal mice. The rise paralleled the onset of anti-DNA antibodies, occurring earlier in females than in males. The increased number of cells was due to an accumulation of medium-sized cells with an intermediate appearance, but with the functional characteristics and cell markers typical of a macrophage. The unusual cells were esterase, F4/80 and Mac-1 positive, peroxidase, and Alcian blue negative, and were shown on sedimentation velocity separation to be phagocytic for EA and C3 (serum-treated) zymosan; 47-48% of peritoneal cells were Ia positive. |
Stephens, R. W.; Golder, J. P.; Fayle, D. R. H.; Hume, D. A.; Hapel, A. J.; Allan, W.; Fordham, C. J.; Doe, W. F. Minactivin expression in human monocyte and macrophage populations (Journal Article) In: Blood, vol. 66, no. 2, pp. 333–337, 1985, ISSN: 00064971. @article{stephens_minactivin_1985,
title = {Minactivin expression in human monocyte and macrophage populations},
author = {R. W. Stephens and J. P. Golder and D. R. H. Fayle and D. A. Hume and A. J. Hapel and W. Allan and C. J. Fordham and W. F. Doe},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021884778&doi=10.1182%2fblood.v66.2.333.bloodjournal662333&partnerID=40&md5=707d23eb276d7ba46c6a56c59e893d9f},
doi = {10.1182/blood.v66.2.333.bloodjournal662333},
issn = {00064971},
year = {1985},
date = {1985-01-01},
journal = {Blood},
volume = {66},
number = {2},
pages = {333--337},
abstract = {Adherent monolayer cultures of human blood monocytes, peritoneal macrophages, bone marrow macrophages, and colonic mucosa macrophages were examined for their ability to produce and secrete minactivin, a specific inactivator of urokinase-type plasminogen activator. All except colonic mucosa macrophages produced and secreted appreciable amounts of minactivin, but only blood monocytes were stimulated by muramyl dipeptide (adjuvant peptide) to increase production. The minactivin from each of these populations could be shown to preferentially inhibit urokinase-type plasminogen activator and not trypsin, plasmin, or 'tissue'-type plasminogen activator (HPA66). A plasminogen-activating enzyme present in monocyte cultures appeared unaffected by the presence of minactivin and could be shown to be regulated independently by dexamethasone.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Adherent monolayer cultures of human blood monocytes, peritoneal macrophages, bone marrow macrophages, and colonic mucosa macrophages were examined for their ability to produce and secrete minactivin, a specific inactivator of urokinase-type plasminogen activator. All except colonic mucosa macrophages produced and secreted appreciable amounts of minactivin, but only blood monocytes were stimulated by muramyl dipeptide (adjuvant peptide) to increase production. The minactivin from each of these populations could be shown to preferentially inhibit urokinase-type plasminogen activator and not trypsin, plasmin, or 'tissue'-type plasminogen activator (HPA66). A plasminogen-activating enzyme present in monocyte cultures appeared unaffected by the presence of minactivin and could be shown to be regulated independently by dexamethasone. |
Summers, K. M.; Hume, D. A. Expression of glandular kallikrein genes in lymphoid and hemopoietic tissues and cell lines (Journal Article) In: Lymphokine Research, vol. 4, no. 3, pp. 229–235, 1985, ISSN: 02776766. @article{summers_expression_1985,
title = {Expression of glandular kallikrein genes in lymphoid and hemopoietic tissues and cell lines},
author = {K. M. Summers and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021877482&partnerID=40&md5=b48740178a771e0d647f7628c31d8098},
issn = {02776766},
year = {1985},
date = {1985-01-01},
journal = {Lymphokine Research},
volume = {4},
number = {3},
pages = {229--235},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
1984
|
Hume, D. A.; Perry, V. H.; Gordon, S. The mononuclear phagocyte system of the mouse defined by immunohistochemical localisation of antigen F4/80: Macrophages associated with epithelia (Journal Article) In: The Anatomical Record, vol. 210, no. 3, pp. 503–512, 1984, ISSN: 0003276X. @article{hume_mononuclear_1984,
title = {The mononuclear phagocyte system of the mouse defined by immunohistochemical localisation of antigen F4/80: Macrophages associated with epithelia},
author = {D. A. Hume and V. H. Perry and S. Gordon},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021716522&doi=10.1002%2far.1092100311&partnerID=40&md5=3a54d42c35b9e9da047e7859d63f2596},
doi = {10.1002/ar.1092100311},
issn = {0003276X},
year = {1984},
date = {1984-01-01},
journal = {The Anatomical Record},
volume = {210},
number = {3},
pages = {503--512},
abstract = {The tissue distribution of the murine macrophage‐specific antigen F4/80 has been analysed using an immunohistochemical technique. The antigen is observed on all known macrophage populations (including Kupffer cells and bronchoalveolar macrophages) and is absent from any cell types that are definitely not mononuclear phagocytes. Microglial cells from brain express F4/80. F4/80+ macrophages observed associated with epithelia can be divided into two categories, intraepithelial and periepithelial. The former includes epidermal Langerhans cells and cells with similar morphology in other stratified squamous epithelia (cervix, oesophagus), pseudostratified epithelium (trachea), transitional epithelium of urinary bladder, and simple epithelia lining various ducts (salivary gland, common bile duct, tracheobronchial gland). Periepithelial F4/80+ cells, apparently spread immediately below the basal lamina, are associated with simple epithelia throughout the gastrointestinal, respiratory, and male and female reproductive tract as well as the brain ependyma. A major class of periepithelial F4/80+ cells is associated with capillaries throughout the microcirulation. The role of these macrophage populations in control of epithelial function is discussed. Copyright © 1984 Wiley‐Liss, Inc.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The tissue distribution of the murine macrophage‐specific antigen F4/80 has been analysed using an immunohistochemical technique. The antigen is observed on all known macrophage populations (including Kupffer cells and bronchoalveolar macrophages) and is absent from any cell types that are definitely not mononuclear phagocytes. Microglial cells from brain express F4/80. F4/80+ macrophages observed associated with epithelia can be divided into two categories, intraepithelial and periepithelial. The former includes epidermal Langerhans cells and cells with similar morphology in other stratified squamous epithelia (cervix, oesophagus), pseudostratified epithelium (trachea), transitional epithelium of urinary bladder, and simple epithelia lining various ducts (salivary gland, common bile duct, tracheobronchial gland). Periepithelial F4/80+ cells, apparently spread immediately below the basal lamina, are associated with simple epithelia throughout the gastrointestinal, respiratory, and male and female reproductive tract as well as the brain ependyma. A major class of periepithelial F4/80+ cells is associated with capillaries throughout the microcirulation. The role of these macrophage populations in control of epithelial function is discussed. Copyright © 1984 Wiley‐Liss, Inc. |
Hume, D. A.; Gordon, S. The correlation between plasminogen activator activity and thymidine incorporation in mouse bone marrow-derived macrophages. Opposing actions of colony-stimulating factor, phorbol myristate acetate, dexamethasone and prostaglandin E (Journal Article) In: Experimental Cell Research, vol. 150, no. 2, pp. 347–355, 1984, ISSN: 00144827. @article{hume_correlation_1984,
title = {The correlation between plasminogen activator activity and thymidine incorporation in mouse bone marrow-derived macrophages. Opposing actions of colony-stimulating factor, phorbol myristate acetate, dexamethasone and prostaglandin E},
author = {D. A. Hume and S. Gordon},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021321676&doi=10.1016%2f0014-4827%2884%2990578-0&partnerID=40&md5=93ed57cde5d04eb2557efaea0a2128a2},
doi = {10.1016/0014-4827(84)90578-0},
issn = {00144827},
year = {1984},
date = {1984-01-01},
journal = {Experimental Cell Research},
volume = {150},
number = {2},
pages = {347--355},
abstract = {Plasminogen activator activity and [3H]thymidine incorporation were studied in mouse bone marrow-derived macrophages. The two activities correlated closely in the presence of stimulatory (colony-stimulating factor, phorbol myristate acetate, PMA) and inhibitory (dexamethasone, prostaglandin E1) signals. The actions of dexamethasone and prostaglandin E1 could be overcome by either stimulatory agent, so that the net effect was an alteration in sensitivity of the macrophages to colony-stimulating factor, or PMA. The sensitivity of bone marrow-derived macrophages to CSF-1 was also reduced by the addition of small numbers of CSF-1 unresponsive peritoneal macrophages. Plasminogen activator induction was not a sufficient signal for [3H]thymidine incorporation which requires an additional macromolecular serum component. The serum component was found not to be plasminogen. © 1984.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Plasminogen activator activity and [3H]thymidine incorporation were studied in mouse bone marrow-derived macrophages. The two activities correlated closely in the presence of stimulatory (colony-stimulating factor, phorbol myristate acetate, PMA) and inhibitory (dexamethasone, prostaglandin E1) signals. The actions of dexamethasone and prostaglandin E1 could be overcome by either stimulatory agent, so that the net effect was an alteration in sensitivity of the macrophages to colony-stimulating factor, or PMA. The sensitivity of bone marrow-derived macrophages to CSF-1 was also reduced by the addition of small numbers of CSF-1 unresponsive peritoneal macrophages. Plasminogen activator induction was not a sufficient signal for [3H]thymidine incorporation which requires an additional macromolecular serum component. The serum component was found not to be plasminogen. © 1984. |
Hume, D. A.; Loutit, J. F.; Gordon, S. The mononuclear phagocyte system of the mouse defined by immunohistochemical localization of antigen F4/80: Macrophages of bone and associated connective tissue (Journal Article) In: Journal of Cell Science, vol. VOL. 66, pp. 189–194, 1984, ISSN: 00219533. @article{hume_mononuclear_1984-1,
title = {The mononuclear phagocyte system of the mouse defined by immunohistochemical localization of antigen F4/80: Macrophages of bone and associated connective tissue},
author = {D. A. Hume and J. F. Loutit and S. Gordon},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021285514&partnerID=40&md5=29b2c9ab797a82eb7e08c776493019f2},
issn = {00219533},
year = {1984},
date = {1984-01-01},
journal = {Journal of Cell Science},
volume = {VOL. 66},
pages = {189--194},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Hapel, A. J.; Warren, H. S.; Hume, D. A. Different colony-stimulating factors are detected by the 'interleukin-3'-dependent cell lines FDC-Pl and 32D cl-23 (Journal Article) In: Blood, vol. 64, no. 4, pp. 786–790, 1984, ISSN: 00064971. @article{hapel_different_1984,
title = {Different colony-stimulating factors are detected by the 'interleukin-3'-dependent cell lines FDC-Pl and 32D cl-23},
author = {A. J. Hapel and H. S. Warren and D. A. Hume},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021193845&doi=10.1182%2fblood.v64.4.786.bloodjournal644786&partnerID=40&md5=74aa889dabdc976bbfc1ff91143f1832},
doi = {10.1182/blood.v64.4.786.bloodjournal644786},
issn = {00064971},
year = {1984},
date = {1984-01-01},
journal = {Blood},
volume = {64},
number = {4},
pages = {786--790},
abstract = {The cell lines FDC-Pl and 32D cl-23 have previously been used as unique indicators for the growth-promoting activity of interleukin-3. We show that FDC-Pl cells respond to granulocyte/macrophage colony-stimulating factor (GM-CSF, CSF-2) as well as to interleukin-3. In keeping with this finding, FDC-Pl cells express the macrophage-specific marker, F4/80. FDC-Pl cells do not, however, respond to macrophage CSF (M-CSF, CSF-1). In contrast, 32D cl-23 cells do not respond to GM-CSF and lack F4/80. Instead, 32D cl-23 cells respond to an as yet undefined factor in conditioned medium (CM) from the primate T cell line, MLA-144, and CM from mitogen-stimulated human lymphocytes (HLCM). 32D cl-23 cells are Lyt-1+. Both FDC-Pl and 32D cl-23 cells consume interleukin-3, but only FDC Pl cells consume GM-CSF. Similarly, 32D cl-23, but not FDC-Pl, cells consume 32D cl-23 growth factor from MLA-144 CM and HLCM. Interleukin-3-dependent cell lines must therefore concurrently express different functional cell surface receptors for a variety of biochemically distinct growth factors.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The cell lines FDC-Pl and 32D cl-23 have previously been used as unique indicators for the growth-promoting activity of interleukin-3. We show that FDC-Pl cells respond to granulocyte/macrophage colony-stimulating factor (GM-CSF, CSF-2) as well as to interleukin-3. In keeping with this finding, FDC-Pl cells express the macrophage-specific marker, F4/80. FDC-Pl cells do not, however, respond to macrophage CSF (M-CSF, CSF-1). In contrast, 32D cl-23 cells do not respond to GM-CSF and lack F4/80. Instead, 32D cl-23 cells respond to an as yet undefined factor in conditioned medium (CM) from the primate T cell line, MLA-144, and CM from mitogen-stimulated human lymphocytes (HLCM). 32D cl-23 cells are Lyt-1+. Both FDC-Pl and 32D cl-23 cells consume interleukin-3, but only FDC Pl cells consume GM-CSF. Similarly, 32D cl-23, but not FDC-Pl, cells consume 32D cl-23 growth factor from MLA-144 CM and HLCM. Interleukin-3-dependent cell lines must therefore concurrently express different functional cell surface receptors for a variety of biochemically distinct growth factors. |
Hume, D. A.; Halpin, D.; Charlton, H.; Gordon, S. The mononuclear phagocyte system of the mouse defined by immunohistochemical localization of antigen F4/80: Macrophages of endocrine organs (Journal Article) In: Proceedings of the National Academy of Sciences of the United States of America, vol. 81, no. 13 I, pp. 4174–4177, 1984, ISSN: 00278424. @article{hume_mononuclear_1984-2,
title = {The mononuclear phagocyte system of the mouse defined by immunohistochemical localization of antigen F4/80: Macrophages of endocrine organs},
author = {D. A. Hume and D. Halpin and H. Charlton and S. Gordon},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0007882598&doi=10.1073%2fpnas.81.13.4174&partnerID=40&md5=f97b04c93faad7342af6185a882faa1b},
doi = {10.1073/pnas.81.13.4174},
issn = {00278424},
year = {1984},
date = {1984-01-01},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {81},
number = {13 I},
pages = {4174--4177},
abstract = {Macrophages of endocrine organs have been identified by immunohistochemical localization of the macrophage-specific antigen F4/80. F4/80+ cells line vascular sinuses and capillaries in anterior and posterior pituitary, adrenal cortex, corpus luteum, parathyroid, pineal gland, and islets of Langerhans. In testis approximately 20% of interstitial cells are F4/80+. F4/80+ cells infiltrate corpus luteum in increased numbers during luteolysis.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Macrophages of endocrine organs have been identified by immunohistochemical localization of the macrophage-specific antigen F4/80. F4/80+ cells line vascular sinuses and capillaries in anterior and posterior pituitary, adrenal cortex, corpus luteum, parathyroid, pineal gland, and islets of Langerhans. In testis approximately 20% of interstitial cells are F4/80+. F4/80+ cells infiltrate corpus luteum in increased numbers during luteolysis. |
1983
|
Hume, D. A.; Robinson, A. P.; Macpherson, G. G.; Gordon, S. The mononuclear phagocyte system of the mouse defined by immunohistochemical localization of antigen F4/80: Relationship between macrophages, langerhans cells, reticular cells, and dendritic cells in lymphoid and hematopoietic organs (Journal Article) In: Journal of Experimental Medicine, vol. 158, no. 5, pp. 1522–1536, 1983, ISSN: 00221007. @article{hume_mononuclear_1983,
title = {The mononuclear phagocyte system of the mouse defined by immunohistochemical localization of antigen F4/80: Relationship between macrophages, langerhans cells, reticular cells, and dendritic cells in lymphoid and hematopoietic organs},
author = {D. A. Hume and A. P. Robinson and G. G. Macpherson and S. Gordon},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021086786&doi=10.1084%2fjem.158.5.1522&partnerID=40&md5=85aae4520bf766166bc756bca84c67f9},
doi = {10.1084/jem.158.5.1522},
issn = {00221007},
year = {1983},
date = {1983-01-01},
journal = {Journal of Experimental Medicine},
volume = {158},
number = {5},
pages = {1522--1536},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Hume, D. A.; Gordon, S.; Thornalley, P. J.; Bannister, J. V. The production of oxygen-centered radicals by Bacillus-Calmette-Guerin-activated macrophages. An electron paramagnetic resonance study of the response to phorbol myristate acetate (Journal Article) In: BBA - Molecular Cell Research, vol. 763, no. 3, pp. 245–250, 1983, ISSN: 01674889. @article{hume_production_1983,
title = {The production of oxygen-centered radicals by Bacillus-Calmette-Guerin-activated macrophages. An electron paramagnetic resonance study of the response to phorbol myristate acetate},
author = {D. A. Hume and S. Gordon and P. J. Thornalley and J. V. Bannister},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021037747&doi=10.1016%2f0167-4889%2883%2990131-3&partnerID=40&md5=578c6b889d330c373ffbfbcb7e744f36},
doi = {10.1016/0167-4889(83)90131-3},
issn = {01674889},
year = {1983},
date = {1983-01-01},
journal = {BBA - Molecular Cell Research},
volume = {763},
number = {3},
pages = {245--250},
abstract = {The spin trapping with 5,5-dimethyl-1-pyrroline-N-oxide of free radicals formed from Bacillus-Calmette-Guerin elicited peritoneal macrophages stimulated with phorbol myristate acetate resulted in the formation of a superoxide and hydroxyl spin adducts. The formation of both spin adducts was inhibited by copper/zinc superoxide dismutase. Only 70% of the hydroxyl spin adduct could be inhibited by catalase or the scavenger dimethyl sulfoxide. This suggests that the production of hydroxyl radicals involves prior formation of both superoxide radicals and hydrogen peroxide, implicating a Fenton catalysed Haber-Weiss reaction. The metal scavenger desferrioxamine also reduced the hydroxyl radical signal by 70%. The unaccounted 30% hydroxyl radical-like signals are probably due to carbon-centered free radicals formed by the lipoxygenase reaction. Spin trapping in the presence of the lipid-soluble spin trap, 5-octadecyl-5,3,3-trimethyl-1-pyrroline-N-oxide, resulted in a spectrum consistent with the presence of an oxaziridine nitroxide. This results from the free radical-induced cyclisation of a nitrone with an unsaturated fatty acid. © 1983.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The spin trapping with 5,5-dimethyl-1-pyrroline-N-oxide of free radicals formed from Bacillus-Calmette-Guerin elicited peritoneal macrophages stimulated with phorbol myristate acetate resulted in the formation of a superoxide and hydroxyl spin adducts. The formation of both spin adducts was inhibited by copper/zinc superoxide dismutase. Only 70% of the hydroxyl spin adduct could be inhibited by catalase or the scavenger dimethyl sulfoxide. This suggests that the production of hydroxyl radicals involves prior formation of both superoxide radicals and hydrogen peroxide, implicating a Fenton catalysed Haber-Weiss reaction. The metal scavenger desferrioxamine also reduced the hydroxyl radical signal by 70%. The unaccounted 30% hydroxyl radical-like signals are probably due to carbon-centered free radicals formed by the lipoxygenase reaction. Spin trapping in the presence of the lipid-soluble spin trap, 5-octadecyl-5,3,3-trimethyl-1-pyrroline-N-oxide, resulted in a spectrum consistent with the presence of an oxaziridine nitroxide. This results from the free radical-induced cyclisation of a nitrone with an unsaturated fatty acid. © 1983. |
Hume, D. A.; Gordon, S. Mononuclear phagocyte system of the mouse defined by immunohistochemical localization of antigen F4/80: Identification of resident macrophages in renal medullary and cortical interstitium and the juxtaglomerular complex (Journal Article) In: Journal of Experimental Medicine, vol. 157, no. 5, pp. 1704–1709, 1983, ISSN: 00221007. @article{hume_mononuclear_1983-1,
title = {Mononuclear phagocyte system of the mouse defined by immunohistochemical localization of antigen F4/80: Identification of resident macrophages in renal medullary and cortical interstitium and the juxtaglomerular complex},
author = {D. A. Hume and S. Gordon},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0020624995&doi=10.1084%2fjem.157.5.1704&partnerID=40&md5=4142060c27a72a2f3aa725f88ed93c9e},
doi = {10.1084/jem.157.5.1704},
issn = {00221007},
year = {1983},
date = {1983-01-01},
journal = {Journal of Experimental Medicine},
volume = {157},
number = {5},
pages = {1704--1709},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Hume, D. A.; Gordon, S. Optimal conditions for proliferation of bone marrow‐derived mouse macrophages in culture: The roles of CSF‐1, serum, Ca2+, and adherence (Journal Article) In: Journal of Cellular Physiology, vol. 117, no. 2, pp. 189–194, 1983, ISSN: 00219541. @article{hume_optimal_1983,
title = {Optimal conditions for proliferation of bone marrow‐derived mouse macrophages in culture: The roles of CSF‐1, serum, Ca2+, and adherence},
author = {D. A. Hume and S. Gordon},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021044136&doi=10.1002%2fjcp.1041170209&partnerID=40&md5=93de6299dbb1846f2aae5b9f3eaa15e4},
doi = {10.1002/jcp.1041170209},
issn = {00219541},
year = {1983},
date = {1983-01-01},
journal = {Journal of Cellular Physiology},
volume = {117},
number = {2},
pages = {189--194},
abstract = {A method is described for the analysis of [3H]‐thymidine incorporation in microtitre cultures of bone marrow‐derived mouse macrophage responding to macrophage colony‐stimulating factor (CSF‐1). [3H]‐thymidine incorporation depends on cell density, culture medium, and the concentration of CSF‐1 and serum, but is independent of Ca2+. Bone marrow‐derived macrophages are strongly adherent, but adherence can be dissociated from [3H]‐thymidine incorporation. Copyright © 1983 Wiley‐Liss, Inc.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
A method is described for the analysis of [3H]‐thymidine incorporation in microtitre cultures of bone marrow‐derived mouse macrophage responding to macrophage colony‐stimulating factor (CSF‐1). [3H]‐thymidine incorporation depends on cell density, culture medium, and the concentration of CSF‐1 and serum, but is independent of Ca2+. Bone marrow‐derived macrophages are strongly adherent, but adherence can be dissociated from [3H]‐thymidine incorporation. Copyright © 1983 Wiley‐Liss, Inc. |
Hume, D. A.; Perry, V. H.; Gordon, S. Immunohistochemical localization of a macrophage-specific antigen in developing mouse retina: Phagocytosis of dying neurons and differentiation in microglial cells to form a regular array in the plexiform layers (Journal Article) In: Journal of Cell Biology, vol. 97, no. 1, pp. 253–257, 1983, ISSN: 00219525. @article{hume_immunohistochemical_1983,
title = {Immunohistochemical localization of a macrophage-specific antigen in developing mouse retina: Phagocytosis of dying neurons and differentiation in microglial cells to form a regular array in the plexiform layers},
author = {D. A. Hume and V. H. Perry and S. Gordon},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-0020536689&doi=10.1083%2fjcb.97.1.253&partnerID=40&md5=23b335dfa67fc3bbf22ba54dd728f717},
doi = {10.1083/jcb.97.1.253},
issn = {00219525},
year = {1983},
date = {1983-01-01},
journal = {Journal of Cell Biology},
volume = {97},
number = {1},
pages = {253--257},
abstract = {In the developing mouse retina degenerating neurons can be observed initially in the ganglion cell layer followed by a phase of cell death in the inner nuclear layer. Using an immunohistochemical method to localize the mouse macrophage specific antigen F4/80, we show that macrophages migrate from the vascular supply overlying the developing retina and phagocytose the degenerating neurons. The macrophages subsequently differentiate to become the microglia of the retina and form a regularly spaced distribution across the retina in the inner and outer plexiform layers. These experiments provide strong evidence for the mesodermal origin of central nervous system microglia.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
In the developing mouse retina degenerating neurons can be observed initially in the ganglion cell layer followed by a phase of cell death in the inner nuclear layer. Using an immunohistochemical method to localize the mouse macrophage specific antigen F4/80, we show that macrophages migrate from the vascular supply overlying the developing retina and phagocytose the degenerating neurons. The macrophages subsequently differentiate to become the microglia of the retina and form a regularly spaced distribution across the retina in the inner and outer plexiform layers. These experiments provide strong evidence for the mesodermal origin of central nervous system microglia. |
