Mechanisms of inflammasome activation: recent advances and novel insights

被引:614
作者
Vanaja, Sivapriya K. [1 ]
Rathinam, Vijay A. K. [1 ]
Fitzgerald, Katherine A. [2 ,3 ]
机构
[1] Univ Connecticut, Ctr Hlth, Dept Immunol, Farmington, CT USA
[2] Univ Massachusetts, Sch Med, Dept Med, Program Innate Immun,Div Infect Dis & Immunol, Worcester, MA 01655 USA
[3] NTNU, Dept Canc Res & Mol Med, Ctr Mol Inflammat Res, N-7491 Trondheim, Norway
关键词
inflammasomes; NLRs; ALRs; non-canonical inflammasome; caspase-11; ANTHRAX LETHAL TOXIN; NLRP3; INFLAMMASOME; CASPASE-1; AUTOPROTEOLYSIS; AIM2; HOST-DEFENSE; CELL-DEATH; ASC; RECEPTORS; MEDIATORS; BACTERIA;
D O I
10.1016/j.tcb.2014.12.009
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Inflammasomes are cytosolic multiprotein platforms assembled in response to invading pathogens and other danger signals. Typically inflammasome complexes contain a sensor protein, an adaptor protein, and a zymogen - procaspase-1. Formation of inflammasome assembly results in processing of inactive procaspase-1 into an active cysteine-protease enzyme, caspase-1, which subsequently activates the proinflammatory cytokines, interleukins IL-1 beta and IL-18, and induces pyroptosis, a highly-pyrogenic inflammatory form of cell death. Studies over the past year have unveiled exciting new players and regulatory pathways that are involved in traditional inflammasome signaling, some of them even challenging the existing dogma. This review outlines these new insights in inflammasome research and discusses areas that warrant further exploration.
引用
收藏
页码:308 / 315
页数:8
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