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• W2889719403 abstract "Abstract Foxp3 + regulatory T cells (Tregs) can inhibit immune responses and maintain immune tolerance by secreting immunosuppressive TGF-β1 and IL-10. However, the efficiency of Tregs become the major obstacle to their use for immunotherapy. In this study, we investigated the relevance of the C-type lectin receptor CD69 to the suppressive function. Compared to CD4 + Foxp3 + CD69 − Tregs (CD69 − Tregs), CD4 + Foxp3 + CD69 + Tregs (CD69 + Tregs) displayed stronger ability to maintain immune tolerance. CD69 + Tregs expressed higher levels of suppression-associated markers such as CTLA-4, ICOS, CD38 and GITR, and secreted higher levels of IL-10 but not TGF-β1. CD69 + Tregs from Il10 +/+ rather than Il10 −/− mice significantly inhibit the proliferation of CD4 + T cells. CD69 over-expression stimulated higher levels of IL-10 and c-Maf expression, which was compromised by silencing of STAT3 or STAT5. In addition, the direct interaction of STAT3 with the c-Maf promoter was detected in cells with CD69 over-expression. Moreover, adoptive transfer of CD69 + Tregs but not CD69 − Tregs or CD69 + Tregs deficient in IL-10 dramatically prevented the development of inflammatory bowel disease (IBD) in mice. Taken together, CD69 is important to the suppressive function of Tregs by promoting IL-10 production. CD69 + Tregs have the potential to develop new therapeutic approach for autoimmune diseases like IBD." @default.
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• W2889719403 date "2018-09-05" @default.
• W2889719403 modified "2023-10-11" @default.
• W2889719403 title "CD69 enhances immunosuppressive function of regulatory T-cells and attenuates colitis by prompting IL-10 production" @default.
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• W2889719403 doi "https://doi.org/10.1038/s41419-018-0927-9" @default.
• W2889719403 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6125584" @default.
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