Molecular Mechanism of NLRP3 Inflammasome Activation

被引:390
作者
Jin, Chengcheng [1 ]
Flavell, Richard A. [1 ,2 ]
机构
[1] Yale Univ, Dept Immunobiol, Sch Med, New Haven, CT 06520 USA
[2] Yale Univ, Howard Hughes Med Inst, Sch Med, New Haven, CT 06520 USA
关键词
NLRP3; inflammasome; agonist; potassium efflux; reactive oxygen species; cathepsin B; INNATE IMMUNE-RESPONSE; NALP3; INFLAMMASOME; CASPASE-1; ACTIVATION; OXIDATIVE STRESS; CATHEPSIN-B; CELL-DEATH; INTERLEUKIN-1-BETA; SECRETION; MONOCYTE; CRYOPYRIN/NALP3;
D O I
10.1007/s10875-010-9440-3
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 an intracellular multimolecular complex that controls caspase-1 activity in the innate immune system. NLRP3, a member of the NLR family of cytosolic pattern recognition receptors, along with the adaptor protein ASC, mediates caspase-1 activation via assembly of the inflammasome in response to various pathogen-derived factors as well as danger-associated molecules. The active NLRP3 inflammasome drives innate immune response towards invading pathogens and cellular damage, and regulates adaptive immune response. Here, we review identified agonists of the NLRP3 inflammasome and the molecular mechanism by which they induce NLRP3 inflammasome activation. Three signaling pathways involving potassium efflux, generation of reactive oxygen species, and cathepsin B release are discussed.
引用
收藏
页码:628 / 631
页数:4
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