期刊
IMMUNITY
卷 33, 期 2, 页码 192-202出版社
CELL PRESS
DOI: 10.1016/j.immuni.2010.07.014
关键词
-
类别
资金
- Deutsche Forschungsgemeinschaft DFG [SFB TR52 TPA1, SFB 548 A6, SFB TR22, GRK 767, GRK 1043]
- International Graduate School of Immunotherapy
- Carl Zeiss Foundation
- Forschungszentrum Immunologie (FZI)
- Asthma Core Facility, JGU Mainz
Interferon-regulatory factor 4 (IRF4) is essential for the development of T helper 2 (Th2) and Th17 cells. Herein, we report that IRF4 is also crucial for the development and function of an interleukin-9 (IL-9)-producing CD4(+) T cell subset designated Th9. IRF4-deficient CD4(+) T cells failed to develop into IL-9-producing Th9 cells, and IRF4-specific siRNA inhibited IL-9 production in wild-type CD4(+) T cells. Chromatin-immunoprecipitation (ChIP) analyses revealed direct IRF4 binding to the II9 promoter in Th9 cells. In a Th9-dependent asthma model, neutralization of IL-9 substantially ameliorated asthma symptoms. The relevance of these findings is emphasized by the fact that the induction of IL-9 production also occurs in human CD4(+) T cells accompanied by the upregulation of IRF4. Our data clearly demonstrate the central function of IRF4 in the development of Th9 cells and underline the contribution of this T helper cell subset to the pathogenesis of asthma.
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