知识与财富的链接
炎症小体是机体固有免疫的重要组成部分,目前对NLRP3炎症小体的研究最为热门和透彻.NLRP3炎症小体的活化因素包括病原体及其分泌的毒素、晶体和内源性危险信号等.NLRP3炎症小体的活化需要启动和激活两个步骤,其中启动机制主要针对NLRP3的转录和翻译后修饰水平,激活机制与线粒体、离子流动和溶酶体等相关.本文还综述了NLRP3炎症小体在表达、组装、活化等方面存在的负调控机制.
The NLRP3 inflammasome is by far the most thoroughly studied of the inflammasome complexes that have been described. NLRP3-activating signals include toxins secreted by pathogens, crystalline molecules and endogenous danger signals. Activation of NLRP3 inflammasome is regulated on the activating and priming steps. The priming step affects NLRP3 at the transcriptional and posttranscriptional modifications levels; the second step is associated with ion flowing, mitochondria or lysosomes. In this paper, we also reviewed the negative regulation of NLRP3 inflammasome at the expression, assembly and activation levels.
