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Macrophage deactivation by interleukin 10.
Open accessAbstract
Recombinant mouse interleukin 10 (IL-10) was exceedingly potent at suppressing the ability of mouse peritoneal macrophages (m phi) to release tumor necrosis factor alpha (TNF-alpha). The IC50 of IL-10 for the suppression of TNF-alpha release induced by 0.5 microgram/ml lipopolysaccharide was 0.04 +/- 0.03 U/ml, with as little as 1 U/ml suppressing TNF-alpha production by a factor of 21.4 +/- 2.5. At 10 U/ml, IL-10 markedly suppressed m phi release of reactive oxygen intermediates (ROI) (IC50 3.7 +/- 1.8 U/ml), but only weakly inhibited m phi release of reactive nitrogen intermediates (RNI). Since TNF-alpha is a T cell growth and differentiation factor, whereas ROI and RNI are known to inhibit lymphocyte function, it is possible that m phi exposed to low concentrations of IL-10 suppress lymphocytes. m phi deactivated by higher concentrations of IL-10 might be permissive for the growth of microbial pathogens and tumor cells, as TNF-alpha, ROI, and RNI are major antimicrobial and tumoricidal products of m phi. IL-10's effects on m phi overlap with but are distinct from the effects of the two previously described cytokines that suppress the function of mouse m phi, transforming growth factor beta and macrophage deactivation factor. Based on results with neutralizing antibodies, all three m phi suppressor factors appear to act independently.
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Metadata
- Authors
- Bogdan, C., Vodovotz, Y., & Nathan, C.
- Venue
- The Journal of experimental medicine
- Publisher
- Rockefeller University Press
- Published
- 1991-12-01
- Volume
- 174
- Issue
- 6
- Pages
- 1549-1555
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2138387587
- Cited by
- 1,238
- References
- 3
- FWCI
- 18.03
- Type
- journal article
- Language
- en
- Open access
- green
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