炎症体
刺
干扰素基因刺激剂
先天免疫系统
细胞生物学
目标2
内质网
分泌物
半胱氨酸蛋白酶1
上睑下垂
生物
吡喃结构域
免疫系统
化学
免疫学
炎症
NLRC4型
NLRP1
生物化学
航空航天工程
工程类
作者
Wenbiao Wang,Dingwen Hu,Chao Wu,Yuqian Feng,Aixin Li,Weiyong Liu,Yingchong Wang,Keli Chen,Mingfu Tian,Feng Xiao,Qi Zhang,Muhammad Adnan Shereen,Weijie Chen,Pan Pan,Pin Wan,Kailang Wu,Jianguo Wu
出处
期刊:PLOS Pathogens
[Public Library of Science]
日期:2020-03-18
卷期号:16 (3): e1008335-e1008335
被引量:109
标识
DOI:10.1371/journal.ppat.1008335
摘要
One of the fundamental reactions of the innate immune responses to pathogen infection is the release of pro-inflammatory cytokines, including IL-1β, processed by the NLRP3 inflammasome. The stimulator of interferon genes (STING) has the essential roles in innate immune response against pathogen infections. Here we reveal a distinct mechanism by which STING regulates the NLRP3 inflammasome activation, IL-1β secretion, and inflammatory responses in human cell lines, mice primary cells, and mice. Interestingly, upon HSV-1 infection and cytosolic DNA stimulation, STING binds to NLRP3 and promotes the inflammasome activation through two approaches. First, STING recruits NLRP3 and facilitates NLRP3 localization in the endoplasmic reticulum, thereby facilitating the inflammasome formation. Second, STING interacts with NLRP3 and attenuates K48- and K63-linked polyubiquitination of NLRP3, thereby promoting the inflammasome activation. Collectively, we demonstrate that the cGAS-STING-NLRP3 signaling is essential for host defense against HSV-1 infection.
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