The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases

被引：1305

作者：

Davis, Beckley K. ^{[1
]}

Wen, Haitao ^{[1
]}

Ting, Jenny P. -Y. ^{[1
]}

机构：

[1] Univ N Carolina, Dept Microbiol & Immunol, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA

来源：

ANNUAL REVIEW OF IMMUNOLOGY, VOL 29 | 2011年 / 29卷

关键词：

innate immunity; metabolic diseases; cancer; IL-1; beta; caspase-1; NF-KAPPA-B; EXTRACELLULAR ATP TRIGGERS; CUTTING EDGE; NALP3; INFLAMMASOME; HOST-DEFENSE; CASPASE-1; ACTIVATION; GENE FAMILY; ENDOGENOUS INHIBITOR; PATTERN-RECOGNITION; INSULIN-RESISTANCE;

D O I：

10.1146/annurev-immunol-031210-101405

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Inflammasome activation leads to caspase-1 activation, which causes the maturation and secretion of pro-IL-1 beta and pro-IL-18 among other substrates. A subgroup of the NLR (nucleotide-binding domain, leucine-rich repeat containing) proteins are key mediators of the inflammasome. Studies of gene-deficient mice and cells have implicated NLR inflammasomes in a host of responses to a wide range of microbial pathogens, inflammatory diseases, cancer, and metabolic and autoinumine disorders. Determining exactly how the inflammasome is activated in these diseases and disease models remains a challenge. This review presents and integrates recent progress in the field.

引用

页码：707 / 735

页数：29

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