INTERLEUKIN 2 DOWN-MODULATES THE MACROPHAGE COLONY-STIMULATING FACTOR RECEPTOR IN MURINE MACROPHAGES
Cytokine, ISSN: 1043-4666, Vol: 8, Issue: 6, Page: 488-494
1996
- 13Citations
- 12Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations13
- Citation Indexes13
- 13
- CrossRef5
- Captures12
- Readers12
- 12
Article Description
Macrophage colony-stimulating factor (M-CSF) is the main growth factor for mononuclear phagocytes. Responsiveness to growth factors is reduced in the course of functional activation of macrophages. We studied the interference of the macrophage activator interleukin 2 (IL-2) with the response to M-CSF, in macrophages of the M-CSF-dependent murine line BAC-1.2F5. Long-term effects of IL-2 on cell growth were determined, showing that IL-2 reduces the M-CSF-dependent proliferation of macrophages. Short-term effects of IL-2 on the expression of the receptor for M-CSF (M-CSF.R) were characterized in more detail. IL-2 rapidly down-modulated M-CSF.R in a dose-dependent fashion, and interferon-γand lipopolysaccharides synergized with IL-2 in this modulation. The IL-2-induced down-modulation of M-CSF.R was shown to require the activity of protein-kinase-C and phospholipase-C. The data are consistent with the hypothesis that the down-modulation of M-CSF.R is a general property of macrophage activators.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1043466696900666; http://dx.doi.org/10.1006/cyto.1996.0066; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0030175396&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/8818546; https://linkinghub.elsevier.com/retrieve/pii/S1043466696900666; https://dx.doi.org/10.1006/cyto.1996.0066
Elsevier BV
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