The Inflammasomes

被引:5108
作者
Schroder, Kate [1 ,2 ]
Tschopp, Jurg [1 ]
机构
[1] Univ Lausanne, Dept Biochem, CH-1066 Epalinges, Switzerland
[2] Monash Univ, Monash Inst Med Res, Melbourne, Vic 3800, Australia
基金
瑞士国家科学基金会; 英国医学研究理事会;
关键词
NF-KAPPA-B; COLD AUTOINFLAMMATORY SYNDROME; RILONACEPT INTERLEUKIN-1 TRAP; ANTHRAX LETHAL TOXIN; NALP3; INFLAMMASOME; CASPASE-1; ACTIVATION; CELL-DEATH; NLRP3; PATTERN-RECOGNITION; OXIDATIVE STRESS;
D O I
10.1016/j.cell.2010.01.040
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Inflammasomes are molecular platforms activated upon cellular infection or stress that trigger the maturation of proinflammatory cytokines such as interleukin-1 beta to engage innate immune defenses. Strong associations between dysregulated inflammasome activity and human heritable and acquired inflammatory diseases highlight the importance this pathway in tailoring immune responses. Here, we comprehensively review mechanisms directing normal inflammasome function and its dysregulation in disease. Agonists and activation mechanisms of the NLRP1, NLRP3, IPAF, and AIM2 inflammasomes are discussed. Regulatory mechanisms that potentiate or limit inflammasome activation are examined, as well as emerging links between the inflammasome and pyroptosis and autophagy.
引用
收藏
页码:821 / 832
页数:12
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