Journal
JOURNAL OF IMMUNOLOGY
Volume 179, Issue 11, Pages 7215-7219Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.179.11.7215
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Funding
- Medical Research Council [G0700128] Funding Source: researchfish
- MRC [G0700128] Funding Source: UKRI
- Medical Research Council [G0700128] Funding Source: Medline
- NCI NIH HHS [P30 CA21765, T32 CA09598-16] Funding Source: Medline
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IL-10 regulates anti-inflammatory signaling via the activation of STA T3, which in turn controls the induction of a gene expression program whose products execute inhibitory effects on proinflammatory mediator production. In this study we show that IL-10 induces the expression of an ETS family transcriptional repressor, ETV3, and a helicase family corepressor, Strawberry notch homologue 2 (SBNO2), in mouse and human macrophages. IL-10-mediated induction of ETV3 and SBNO2 expression was dependent upon both STAT3 and a stimulus through the TLR pathway. We also observed that ETV3 expression was strongly induced by the STAT3 pathway regulated by IL-10 but not by STAT3 signaling activated by IL-6, which cannot activate the anti-inflammatory signaling pathway. ETV3 and SBNO2 repressed NF-kappa B- but not IFN regulatory factor 7 (IRF7)-activated transcriptional reporters. Collectively our data suggest that ETV3 and SBNO2 are components of the pathways that contribute to the downstream anti-inflammatory effects of IL-10.
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