Mechanisms of NOD-like Receptor-Associated Inflammasome Activation

被引：369
|
作者：
Wen, Haitao [1 ]
Miao, Edward A. [1 ,2 ]
Ting, Jenny P. -Y. [1 ,2 ]
机构：
[1] Univ N Carolina, Lineberger Canc Res Ctr, Chapel Hill, NC 27599 USA
[2] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA
来源：
IMMUNITY | 2013年 / 39卷 / 03期
基金：
美国国家卫生研究院;
关键词：
NF-KAPPA-B; ENDOPLASMIC-RETICULUM STRESS; THIOREDOXIN-INTERACTING PROTEIN; INNATE IMMUNE DETECTION; LINKS OXIDATIVE STRESS; NLRP3; INFLAMMASOME; CUTTING EDGE; HOST-DEFENSE; IL-1-BETA SECRETION; COLON INFLAMMATION;
D O I：
10.1016/j.immuni.2013.08.037
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
A major function of a subfamily of NLR (nucleotide-binding domain, leucine-rich repeat containing, or NOD-like receptor) proteins is in inflammasome activation, which has been implicated in a multitude of disease models and human diseases. This work will highlight key progress in understanding the mechanisms that activate the best-studied NLRs (NLRP3, NLRC4, NAIP, and NLRP1) and in uncovering inflammasome NLRs.
引用
收藏
页码：432 / 441
页数：10
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