Negative regulation of NLRP3 inflammasome signaling

被引：70
作者：
Chen, Shuzhen [1 ]
Sun, Bing [1 ,2 ]
机构：
[1] Chinese Acad Sci, Shanghai Inst Biol Sci, State Key Lab Cell Biol, Inst Biochem & Cell Biol, Shanghai 200031, Peoples R China
[2] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Pasteur Shanghai, Key Lab Mol Virol & Immunol, Shanghai 200025, Peoples R China
来源：
PROTEIN & CELL | 2013年 / 4卷 / 04期
关键词：
inflammasome; NLRP3; negative regulation; inflammation; COLD AUTOINFLAMMATORY SYNDROME; NITRIC-OXIDE; NALP3; INFLAMMASOME; IL-1-BETA PRODUCTION; IMMUNE-RESPONSES; DOMAIN PROTEIN; URIC-ACID; ACTIVATION; INNATE; INTERLEUKIN-1-BETA;
D O I：
10.1007/s13238-013-2128-8
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Inflammasomes are multiprotein complexes that serve as a platform for caspase-1 activation and interleukin-1 beta (IL-1 beta) maturation as well as pyroptosis. Though a number of inflammasomes have been described, the NLRP3 inflammasome is the most extensively studied. NLRP3 inflammasome is triggered by a variety of stimuli, including infection, tissue damage and metabolic dysregulation, and then activated through an integrated cellular signal. Many regulatory mechanisms have been identified to attenuate NLRP3 inflammasome signaling at multiple steps. Here, we review the developments in the negative regulation of NLRP3 inflammasome that protect host from inflammatory damage.
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收藏
页码：251 / 258
页数：8
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