Activation and regulation of the inflammasomes

被引:2323
作者
Latz, Eicke [1 ,2 ,3 ,4 ,5 ]
Xiao, T. Sam [6 ]
Stutz, Andrea [1 ]
机构
[1] Univ Bonn, Univ Hosp, Inst Innate Immun, D-53127 Bonn, Germany
[2] Univ Massachusetts, Sch Med, Dept Med, Worcester, MA 01655 USA
[3] Univ Massachusetts, Sch Med, Div Infect Dis & Immunol, Worcester, MA 01655 USA
[4] DZNE, D-53175 Bonn, Germany
[5] Norwegian Univ Sci & Technol, Ctr Mol Inflammat Res, NO-7491 Trondheim, Norway
[6] NIAID, Struct Immunobiol Unit, Immunol Lab, NIH, Bethesda, MD 20892 USA
基金
美国国家卫生研究院;
关键词
NF-KAPPA-B; NOD-LIKE RECEPTOR; NLRP3; INFLAMMASOME; NALP3; CYTOCHROME-C; INTERLEUKIN-1-BETA RELEASE; CASPASE-1; ACTIVATION; IL-1-BETA PRODUCTION; ADAPTIVE IMMUNITY; AIM2;
D O I
10.1038/nri3452
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 key signalling platforms that detect pathogenic microorganisms and sterile stressors, and that activate the highly pro-inflammatory cytokines interleukin-1 beta (IL-1 beta) and IL-18. In this Review, we discuss the complex regulatory mechanisms that facilitate a balanced but effective inflammasome-mediated immune response, and we highlight the similarities to another molecular signalling platform - the apoptosome - that monitors cellular health. Extracellular regulatory mechanisms are discussed, as well as the intracellular control of inflammasome assembly, for example, via ion fluxes, free radicals and autophagy.
引用
收藏
页码:397 / 411
页数:15
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