期刊
IMMUNITY
卷 40, 期 3, 页码 342-354出版社
CELL PRESS
DOI: 10.1016/j.immuni.2014.02.006
关键词
-
类别
资金
- NIH/NCI [P30CA016672]
- National Institutes of Health [AI057555, AI064639, AI104519, GM84459]
Production of type I interferons (IFN-I) is a crucial innate immune mechanism against viral infections. IFN-I induction is subject to negative regulation by both viral and cellular factors, but the underlying mechanism remains unclear. We report that the noncanonical NF-kappa B pathway was stimulated along with innate immune cell differentiation and viral infections and had a vital role in negatively regulating IFN-I induction. Genetic deficiencies in major components of the noncanonical NF-kappa B pathway caused IFN-I hyperinduction and rendered cells and mice substantially more resistant to viral infection. Noncanonical NF-kappa B suppressed signal-induced histone modifications at the Ifnb promoter, an action that involved attenuated recruitment of the transcription factor RelA and a histone demethylase, JMJD2A. These findings reveal an unexpected function of the noncanonical NF-kappa B pathway and highlight an important mechanism regulating antiviral innate immunity.
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