期刊
JOURNAL OF IMMUNOLOGY
卷 179, 期 6, 页码 3724-3733出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.179.6.3724
关键词
-
类别
资金
- NIAID NIH HHS [AI063064] Funding Source: Medline
In this study, we report a novel biological function of vitamin A metabolites in conversion of naive FoxP3(-) CD4(+) T cells into a unique FoxP3(+) regulatory T cell subset (termed retinoid-induced FoxP3(+) T cells) in both human and mouse T cells. We found that the major vitamin A metabolite all-traps-retinoic acid induces histone acetylation at the FoxP3 gene promoter and expression of the FoxP3 protein in CD4+ T cells. The induction of retinoid-induced FoxP3(+) T cells is mediated by the nuclear retinoic acid receptor a and involves T cell activation driven by mucosal dendritic cells and costimulation through CD28. Retinoic acid can promote TGF-beta 1-dependent generation of FoxP3(+) regulatory T cells but decrease the TGF-beta 1- and IL-6-dependent generation of inflammatory Th17 cells in mouse T cells. Retinoid-induced FoxP3(+) T cells can efficiently suppress target cells and, thus, have a regulatory function typical for FoxP3(+) T cells. A unique cellular feature of these regulatory T cells is their high expression of gut-homing receptors that are important for migration to the mucosal tissues particularly the small intestine. Taken together, these results identify retinoids as positive regulatory factors for generation of gut-homing FoxP3(+) T cells.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据