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Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferati...
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Zeitschriftentitel: | Blood |
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Personen und Körperschaften: | , |
In: | Blood, 75, 1990, 8, S. 1627-1632 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
American Society of Hematology
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Schlagwörter: |
author_facet |
Chen, BD Mueller, M Chen, BD Mueller, M |
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author |
Chen, BD Mueller, M |
spellingShingle |
Chen, BD Mueller, M Blood Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor Cell Biology Hematology Immunology Biochemistry |
author_sort |
chen, bd |
spelling |
Chen, BD Mueller, M 0006-4971 1528-0020 American Society of Hematology Cell Biology Hematology Immunology Biochemistry http://dx.doi.org/10.1182/blood.v75.8.1627.bloodjournal7581627 <jats:p>Tumor necrosis factor (TNF) is a protein produced by activated macrophages in response to endotoxin. The effect of recombinant murine TNF (rMuTNF) on the growth of murine tissue-derived macrophage colony- forming units (CFU-M) which are responsive to both macrophage and granulocyte-macrophage colony-stimulating factors (M-CSF and GM-CSF), was studied. TNF alone did not stimulate macrophage proliferation but did prolong their survival in vitro. The proliferative response of CFU- M to M-CSF, however, was greatly enhanced by the presence of TNF. The enhancement effect of TNF is dose-dependent, reaching a maximum at approximately 50 U/mL. In contrast, the proliferative responsiveness of CFU-M to GM-CSF was inhibited by the concurrent addition of rMuTNF. Both effects appear to be caused directly by rMuTNF, rather than by the secondary factor(s) produced by TNF-treated macrophages. TNF treatment also induced a transient downmodulation of M-CSF receptors in cultured macrophages and accelerated their uptake and use of exogenous M-CSF, which may account for, at least in part, the enhanced proliferative activity in response to M-CSF. Short-term treatment (24 hours) was not sufficient to induce either an enhancing or an inhibitory effect upon CFU-M. This study suggests an autoregulatory role for TNF in the production of mature tissue macrophages by selectively enhancing their proliferative response to lineage specific growth factor, M-CSF.</jats:p> Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor Blood |
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10.1182/blood.v75.8.1627.bloodjournal7581627 |
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Biologie Medizin Chemie und Pharmazie |
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American Society of Hematology, 1990 |
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American Society of Hematology, 1990 |
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0006-4971 1528-0020 |
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American Society of Hematology (CrossRef) |
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1990 |
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American Society of Hematology |
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Blood |
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title |
Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor |
title_unstemmed |
Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor |
title_full |
Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor |
title_fullStr |
Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor |
title_full_unstemmed |
Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor |
title_short |
Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor |
title_sort |
recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor |
topic |
Cell Biology Hematology Immunology Biochemistry |
url |
http://dx.doi.org/10.1182/blood.v75.8.1627.bloodjournal7581627 |
publishDate |
1990 |
physical |
1627-1632 |
description |
<jats:p>Tumor necrosis factor (TNF) is a protein produced by activated macrophages in response to endotoxin. The effect of recombinant murine TNF (rMuTNF) on the growth of murine tissue-derived macrophage colony- forming units (CFU-M) which are responsive to both macrophage and granulocyte-macrophage colony-stimulating factors (M-CSF and GM-CSF), was studied. TNF alone did not stimulate macrophage proliferation but did prolong their survival in vitro. The proliferative response of CFU- M to M-CSF, however, was greatly enhanced by the presence of TNF. The enhancement effect of TNF is dose-dependent, reaching a maximum at approximately 50 U/mL. In contrast, the proliferative responsiveness of CFU-M to GM-CSF was inhibited by the concurrent addition of rMuTNF. Both effects appear to be caused directly by rMuTNF, rather than by the secondary factor(s) produced by TNF-treated macrophages. TNF treatment also induced a transient downmodulation of M-CSF receptors in cultured macrophages and accelerated their uptake and use of exogenous M-CSF, which may account for, at least in part, the enhanced proliferative activity in response to M-CSF. Short-term treatment (24 hours) was not sufficient to induce either an enhancing or an inhibitory effect upon CFU-M. This study suggests an autoregulatory role for TNF in the production of mature tissue macrophages by selectively enhancing their proliferative response to lineage specific growth factor, M-CSF.</jats:p> |
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author | Chen, BD, Mueller, M |
author_facet | Chen, BD, Mueller, M, Chen, BD, Mueller, M |
author_sort | chen, bd |
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container_start_page | 1627 |
container_title | Blood |
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description | <jats:p>Tumor necrosis factor (TNF) is a protein produced by activated macrophages in response to endotoxin. The effect of recombinant murine TNF (rMuTNF) on the growth of murine tissue-derived macrophage colony- forming units (CFU-M) which are responsive to both macrophage and granulocyte-macrophage colony-stimulating factors (M-CSF and GM-CSF), was studied. TNF alone did not stimulate macrophage proliferation but did prolong their survival in vitro. The proliferative response of CFU- M to M-CSF, however, was greatly enhanced by the presence of TNF. The enhancement effect of TNF is dose-dependent, reaching a maximum at approximately 50 U/mL. In contrast, the proliferative responsiveness of CFU-M to GM-CSF was inhibited by the concurrent addition of rMuTNF. Both effects appear to be caused directly by rMuTNF, rather than by the secondary factor(s) produced by TNF-treated macrophages. TNF treatment also induced a transient downmodulation of M-CSF receptors in cultured macrophages and accelerated their uptake and use of exogenous M-CSF, which may account for, at least in part, the enhanced proliferative activity in response to M-CSF. Short-term treatment (24 hours) was not sufficient to induce either an enhancing or an inhibitory effect upon CFU-M. This study suggests an autoregulatory role for TNF in the production of mature tissue macrophages by selectively enhancing their proliferative response to lineage specific growth factor, M-CSF.</jats:p> |
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spelling | Chen, BD Mueller, M 0006-4971 1528-0020 American Society of Hematology Cell Biology Hematology Immunology Biochemistry http://dx.doi.org/10.1182/blood.v75.8.1627.bloodjournal7581627 <jats:p>Tumor necrosis factor (TNF) is a protein produced by activated macrophages in response to endotoxin. The effect of recombinant murine TNF (rMuTNF) on the growth of murine tissue-derived macrophage colony- forming units (CFU-M) which are responsive to both macrophage and granulocyte-macrophage colony-stimulating factors (M-CSF and GM-CSF), was studied. TNF alone did not stimulate macrophage proliferation but did prolong their survival in vitro. The proliferative response of CFU- M to M-CSF, however, was greatly enhanced by the presence of TNF. The enhancement effect of TNF is dose-dependent, reaching a maximum at approximately 50 U/mL. In contrast, the proliferative responsiveness of CFU-M to GM-CSF was inhibited by the concurrent addition of rMuTNF. Both effects appear to be caused directly by rMuTNF, rather than by the secondary factor(s) produced by TNF-treated macrophages. TNF treatment also induced a transient downmodulation of M-CSF receptors in cultured macrophages and accelerated their uptake and use of exogenous M-CSF, which may account for, at least in part, the enhanced proliferative activity in response to M-CSF. Short-term treatment (24 hours) was not sufficient to induce either an enhancing or an inhibitory effect upon CFU-M. This study suggests an autoregulatory role for TNF in the production of mature tissue macrophages by selectively enhancing their proliferative response to lineage specific growth factor, M-CSF.</jats:p> Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor Blood |
spellingShingle | Chen, BD, Mueller, M, Blood, Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor, Cell Biology, Hematology, Immunology, Biochemistry |
title | Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor |
title_full | Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor |
title_fullStr | Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor |
title_full_unstemmed | Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor |
title_short | Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor |
title_sort | recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor |
title_unstemmed | Recombinant tumor necrosis factor enhances the proliferative responsiveness of murine peripheral macrophages to macrophage colony- stimulating factor but inhibits their proliferative responsiveness to granulocyte-macrophage colony-stimulating factor |
topic | Cell Biology, Hematology, Immunology, Biochemistry |
url | http://dx.doi.org/10.1182/blood.v75.8.1627.bloodjournal7581627 |