Regulation of inflammasome signaling

被引:786
作者
Rathinam, Vijay A. K. [1 ]
Vanaja, Sivapriya Kailasan [1 ,2 ]
Fitzgerald, Katherine A. [1 ]
机构
[1] Univ Massachusetts, Sch Med, Dept Med, Div Infect Dis & Immunol, Worcester, MA 01605 USA
[2] Tufts Sch Med, Dept Microbiol, Boston, MA USA
基金
美国国家卫生研究院;
关键词
NF-KAPPA-B; INNATE IMMUNE RECOGNITION; NLRP3; INFLAMMASOME; CASPASE-1; ACTIVATION; NALP3; CUTTING EDGE; HOST-DEFENSE; LISTERIA-MONOCYTOGENES; AIM2; ONLY PROTEIN-2;
D O I
10.1038/ni.2237
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Innate immune responses have the ability to both combat infectious microbes and drive pathological inflammation. Inflammasome complexes are a central component of these processes through their regulation of interleukin 1 beta (IL-1 beta), IL-18 and pyroptosis. Inflammasomes recognize microbial products or endogenous molecules released from damaged or dying cells both through direct binding of ligands and indirect mechanisms. The potential of the IL-1 family of cytokines to cause tissue damage and chronic inflammation emphasizes the importance of regulating inflammasomes. Many regulatory mechanisms have been identified that act as checkpoints for attenuating inflammasome signaling at multiple steps. Here we discuss the various regulatory mechanisms that have evolved to keep inflammasome signaling in check to maintain immunological balance.
引用
收藏
页码:333 / 342
页数:10
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