期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 37, 期 9, 页码 2396-2399出版社
WILEY-V C H VERLAG GMBH
DOI: 10.1002/eji.200737621
关键词
autoimmunity; retinoic acid; transcription factors
类别
资金
- NIAID NIH HHS [AI42370] Funding Source: Medline
- NIDDK NIH HHS [DK43806] Funding Source: Medline
Autoimmunity is thought to reflect an imbalance between regulatory T helper lymphocytes (Treg) and pathogenic, IL-17-secreting T helper (Th17) cells. Induction of both adaptive Treg and Th17 cells requires signalling from TGF-beta. We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Using a specific agonist and antagonist, as well as retroviral over-expression, we also provide evidence that the effects of ATRA are likely to be at least partially mediated by the nuclear retinoic acid receptor-a, (RAR alpha). These findings indicate that signalling through a specific nuclear retinoic acid receptor can favour the decision to adopt the Treg fate at the expense of Th17 fate. Specific agonists of RAR alpha could, therefore, be considered candidates for the treatment of autoimmunity.
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