Macrophage deactivation by interleukin 10

Christian Bogdan*, Yoram Vodovotz, Carl Nathan

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

1195 Scopus citations

Abstract

Recombinant mouse interleukin 10 (IL-10) was exceedingly potent at suppressing the ability of mouse peritoneal macrophages (mø) to release tumor necrosis factor α (TNF-α). The IC50 of IL-10 for the suppression of TNF-α release induced by 0.5 μg/ml lipopolysaccharide was 0.04 ± 0.03 U/ml, with as little as 1 U/ml suppressing TNF-α production by a factor of 21.4 ± 2.5. At 10 U/ml, IL-10 markedly suppressed mø release of reactive oxygen intermediates (ROI) (IC50 3.7 ±1.8 U/ml), but only weakly inhibited mø release of reactive nitrogen intermediates (RNI). Since TNF-α is a T cell growth and differentiation factor, whereas ROI and RNI are known to inhibit lymphocyte function, it is possible that mø exposed to low concentrations of IL-10 suppress lymphocytes, mø deactivated by higher concentrations of IL-10 might be permissive for the growth of microbial pathogens and tumor cells, as TNF-α, ROI, and RNI are major antimicrobial and tumoricidal products of mø IL-10's effects on mø overlap with but are distinct from the effects of the two previously described cytokines that suppress the function of mouse mø, transforming growth factor β and macrophage deactivation factor. Based on results with neutralizing antibodies, all three mø suppressor factors appear to act independently.

Original languageEnglish
Pages (from-to)1549-1555
Number of pages7
JournalJournal of Experimental Medicine
Volume174
Issue number6
StatePublished - 1 Dec 1991
Externally publishedYes

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