期刊
JOURNAL OF IMMUNOLOGY
卷 202, 期 4, 页码 1039-1044出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1801266
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资金
- University of Alabama School of Medicine
- National Institutes of Health (NIH) Immunology T32 Training Grant [2T32AI007051]
- NIH [P30 CA013148, P30 AR048311, P30 AI027667]
The ICOS pathway has been implicated in the development and functions of regulatory T (Treg) cells, including those producing IL-10. Treg cell-derived IL-10 is indispensable for the establishment and maintenance of intestinal immune homeostasis. We examined the possible involvement of the ICOS pathway in the accumulation of murine colonic Foxp3- and/or IL-10-expressing cells. We show that ICOS deficiency does not impair induction of IL-10 by intestinal CD4 T cells but, instead, triggers substantial reductions in gut-resident and peripherally derived Foxp3(+) Treg cells. ICOS deficiency is associated with reduced demethylation of Foxp3 CNS2 and enhanced loss of Foxp3. This instability significantly limits the ability of ICOS-deficient Treg cells to reverse ongoing inflammation. Collectively, our results identify a novel role for ICOS costimulation in imprinting the functional stability of Foxp3 that is required for the retention of full Treg cell function in the periphery.
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