期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 48, 期 11, 页码 1817-1825出版社
WILEY
DOI: 10.1002/eji.201847589
关键词
Antiviral innate immunity; NLRP2; TBK1; Type I interferons
类别
资金
- National Natural Science Foundation of China [31700777]
Nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) are intracellular pattern recognition receptors (PRRs) that regulate a variety of inflammatory and host defense responses. Unlike the well-established NLRs, the roles of NLRP2 are controversial and poorly defined. Here, we report that NLRP2 acts as a negative regulator of TANK-binding kinase 1 (TBK1)-mediated type I interferon (IFN) signaling. Mechanistically, NLRP2 interacted directly with TBK1, and this binding disrupted the interaction of TBK1 and interferon regulatory factor 3 (IRF3), which interfered with TBK1-induced IRF3 phosphorylation. IFNs induce a series of proteins that have well-known antiviral or immune-regulatory functions, and tight control of the IFN signaling cascade is critical for limiting tissue damage and preventing autoimmunity. Our studies indicate that the NLRP2-TBK1 axis may serve as an additional signaling cascade to maintain immune homeostasis in response to viral infection.
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