The inflammasome: a caspase-1-activation platform that regulates immune responses and disease pathogenesis

被引：1489

作者：

Franchi, Luigi

Eigenbrod, Tatjana

Munoz-Planillo, Raul

Nunez, Gabriel ^{[1
]}

机构：

[1] Univ Michigan, Sch Med, Ctr Comprehens Canc, Dept Pathol, Ann Arbor, MI 48109 USA

来源：

NATURE IMMUNOLOGY | 2009年 / 10卷 / 03期

基金：

美国国家卫生研究院;

关键词：

NF-KAPPA-B; NOD-LIKE RECEPTORS; MUCKLE-WELLS-SYNDROME; CASPASE-1; ACTIVATION; NALP3; INFLAMMASOME; HOST-DEFENSE; LISTERIA-MONOCYTOGENES; MURAMYL DIPEPTIDE; P2X(7) RECEPTOR; INNATE IMMUNITY;

D O I：

10.1038/ni.1703

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The inflammasome is a multiprotein complex that mediates the activation of caspase-1, which promotes secretion of the proinflammatory cytokines interleukin 1 beta (IL-1 beta) and IL-18, as well as 'pyroptosis', a form of cell death induced by bacterial pathogens. Members of the Nod-like receptor family, including NLRP1, NLRP3 and NLRC4, and the adaptor ASC are critical components of the inflammasome that link microbial and endogenous 'danger' signals to caspase-1 activation. Several diseases are associated with dysregulated activation of caspase-1 and secretion of IL-1 beta. Thus, understanding inflammasome pathways may provide insight into disease pathogenesis that might identify potential targets for therapeutic intervention.

引用

收藏

页码：241 / 247

页数：7

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