Sensing damage by the NLRP3 inflammasome

被引:225
作者
Leemans, Jaklien C. [2 ]
Cassel, Suzanne L. [1 ,4 ,5 ]
Sutterwala, Fayyaz S. [1 ,3 ,5 ]
机构
[1] Univ Iowa, Coralville, IA 52241 USA
[2] Univ Amsterdam, Acad Med Ctr, Dept Pathol, NL-1105 AZ Amsterdam, Netherlands
[3] Univ Iowa, Dept Internal Med, Div Infect Dis, Iowa City, IA 52242 USA
[4] Univ Iowa, Dept Internal Med, Div Immunol, Iowa City, IA 52242 USA
[5] Univ Iowa, Dept Internal Med, Inflammat Program, Iowa City, IA 52242 USA
关键词
NLRP3; inflammasome; caspase-1; sterile inflammation; INTERLEUKIN-1 RECEPTOR ANTAGONIST; ISCHEMIA-REPERFUSION INJURY; MUCKLE-WELLS-SYNDROME; COLD AUTOINFLAMMATORY SYNDROME; ACUTE MYOCARDIAL-INFARCTION; PROGRESSIVE RENAL INJURY; INNATE IMMUNE-RESPONSE; NALP3; INFLAMMASOME; ISCHEMIA/REPERFUSION INJURY; ACTIVATES CASPASE-1;
D O I
10.1111/j.1600-065X.2011.01043.x
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 NLRP3 inflammasome is activated in response to a variety of signals that are indicative of damage to the host including tissue damage, metabolic stress, and infection. Upon activation, the NLRP3 inflammasome serves as a platform for activation of the cysteine protease caspase-1, which leads to the processing and secretion of the proinflammatory cytokines interleukin-1 beta (IL-1 beta) and IL-18. Dysregulated NLRP3 inflammasome activation is associated with both heritable and acquired inflammatory diseases. Here, we review new insights into the mechanism of NLRP3 inflammasome activation and its role in disease pathogenesis.
引用
收藏
页码:152 / 162
页数:11
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