期刊
JOURNAL OF IMMUNOLOGY
卷 205, 期 6, 页码 1497-1502出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.2000136
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资金
- National Natural Science Foundation of China [81830051, 31525008, 31961133011, 31670911, 81602558, 31670885]
- National Science Foundation for Young Scientist of China [31800744]
- National Key Research and Development Project [2019YFA0906102]
- Shanghai Jiao Tong University-The Chinese University of Hong Kong Joint Research Collaboration Fund
- Fundamental Research Funds for Central Universities
IL-10 is critical for Foxp3(+) regulatory T cell (Tregs)-mediated immune suppression, but how to efficiently upregulate IL-10 production in Tregs remains unclear. In this article, we show that human IL-10(+) FOXP3(+)-induced regulatory T cell (iTreg) generation can be dramatically promoted by inhibiting GSK3 activity. IL-10+ FOXP3(+) iTregs induced by GSK3 inhibition exhibit classical features of immune-suppressive T cells. We further demonstrate that IL-10(+) iTregs exhibit enhanced suppressive function in both IL-10-dependent and -independent manners. The enhanced suppressive function of IL-10(+) Tregs is not due to a single factor such as IL-10, although IL-10 may mediate this enhanced suppressive function to some extent. Mechanistically, the increased transcriptional activity of IL-10 promoter and the enhanced expression of C-Maf and BLIMP1 coordinately facilitate IL-10 expression in human iTregs under GSK3 inhibition. Our study provides a new strategy to generate human immune-suppressive IL-10(+) FOXP3(+) Tregs for immunotherapies.
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