期刊
JOURNAL OF IMMUNOLOGY
卷 178, 期 11, 页码 6725-6729出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.178.11.6725
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- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [Z01AI000872, ZIAAI000872] Funding Source: NIH RePORTER
Recent studies have shown that TGF-beta together with IL-6 induce the differentiation of IL-17-producing T cells (Th17) T cells. We therefore examined whether CD4(+)CD25(+)Foxp3(+) regulatory T cells, i.e., cells previously shown to produce TGF-beta, serve as Th 17 inducers. We found that upon activation purified CD25(+) T cells (or sorted GFP(+) T cells obtained from Foxp3-GFP knockin mice) produce high amounts of soluble TGF-beta and when cultured with CD4(+) CD25(+)FoxP3(-) T cells in the presence of IL-6 induce the latter to differentiate into Th17 cells. Perhaps more importantly, upon activation, CD4+ CD25(+)Foxp3(+) (GFP(+)) T cells themselves differentiate into Th17 cells in the presence of IL-6 (and in the absence of exogenous TGF-beta). These results indicate that CD4+ CD25+Foxp3+ regulatory T cells can function as inducers of Th17 cells and can differentiate into Th17 cells. They thus have important implications to our understanding of regulatory T cell function and their possible therapeutic use.
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