Sensing and reacting to microbes through the inflammasomes

被引:857
作者
Franchi, Luigi
Munoz-Planillo, Raul
Nunez, Gabriel [1 ]
机构
[1] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA
基金
美国国家卫生研究院;
关键词
NOD-LIKE RECEPTORS; NLRP3; INFLAMMASOME; CASPASE-1; ACTIVATION; LISTERIA-MONOCYTOGENES; HOST-DEFENSE; DIFFERENTIAL REQUIREMENT; NALP3; CELL-DEATH; INTERLEUKIN-1-BETA RELEASE; NEUTROPHIL RECRUITMENT;
D O I
10.1038/ni.2231
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Inflammasomes are multiprotein complexes that activate caspase-1, which leads to maturation of the proinflammatory cytokines interleukin 1 beta (IL-1 beta) and IL-18 and the induction of pyroptosis. Members of the Nod-like receptor (NLR) family, including NLRP1, NLRP3 and NLRC4, and the cytosolic receptor AIM2 are critical components of inflammasomes and link microbial and endogenous danger signals to the activation of caspase-1. In response to microbial infection, activation of the inflammasomes contributes to host protection by inducing immune responses that limit microbial invasion, but deregulated activation of inflanimasomes is associated with autoinflammatory syndromes and other pathologies. Thus, understanding inflammasome pathways may provide insight into the mechanisms of host defense against microbes and the development of inflammatory disorders.
引用
收藏
页码:325 / 332
页数:8
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