4.5 Article

IFN-γ-STAT1 signal regulates the differentiation of inducible Treg: Potential role for ROS-mediated apoptosis

期刊

EUROPEAN JOURNAL OF IMMUNOLOGY
卷 39, 期 5, 页码 1241-1251

出版社

WILEY
DOI: 10.1002/eji.200838913

关键词

Apoptosis; CD4(+) T cells; Treg; ROS

资金

  1. Korean Science and Engineering Foundation [R11-2002-098-08001-0]
  2. Korean government (MEST) [R0A-2008-000-20113-0]
  3. National Research Foundation of Korea [R0A-2008-000-20113-0, R11-2002-098-08001-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

Regulatory CD4(+) T cells are important for the homeostasis of immune cells, and their absence correlates with autoimmune disorders. However, how the immune system regulates Treg homeostasis remains unclear. We found that IFN-gamma-deficient-mice had more forkhead box P3 (FOXP3(+)) cells than WT mice in all secondary lymphoid organs except the thymus. However, T-bet- or IL-4R alpha-deficient mice did not show a similar increase. In vitro differentiation studies showed that conversion of naive T cells into FOXP3(+) cells (neo-generated inducible Treg (iTreg)) by TGF-beta was significantly inhibited by IFN-gamma in a STAT-1-dependent manner. Moreover, an in vivo adoptive transfer study showed that inhibition of FOXP3(+) iTreg generation by IFN-gamma was a T-cell autocrine effect. This inhibitory effect of IFN-gamma on iTreg generation was significantly abrogated after N-acetyl-L-cysteine treatment both in vitro and in vivo, indicating that IFN-gamma regulation of iTreg generation is dependent on ROS-mediated apoptosis. Therefore, our results suggest that autocrine IFN-gamma can negatively regulate the neo-generation of FOXP3(+) iTreg through ROS-mediated apoptosis in the periphery.

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。

评论

主要评分

4.5
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据