Molecular Mechanism of NLRP3 Inflammasome Activation
Molecular Mechanism of NLRP3 Inflammasome Activation
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DOI：
10.1007/s10875-010-9440-3
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发表时间：
2010-09-01
影响因子：
9.1
通讯作者：
Flavell, Richard A.
中科院分区：
文献类型：
--
作者：
Jin, Chengcheng;Flavell, Richard A.
炎症小体是一种细胞内多分子复合物，控制先天免疫系统中的 caspase-1 活性。 NLRP3 是胞质模式识别受体 NLR 家族的成员，与接头蛋白 ASC 一起，通过组装炎症小体来介导 caspase-1 激活，以响应各种病原体衍生因子以及危险相关分子。活跃的 NLRP3 炎性体可驱动针对入侵病原体和细胞损伤的先天免疫反应，并调节适应性免疫反应。在这里，我们回顾了已鉴定的 NLRP3 炎症小体激动剂及其诱导 NLRP3 炎症小体激活的分子机制。讨论了涉及钾流出、活性氧生成和组织蛋白酶 B 释放的三种信号传导途径。
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.