NLRP3炎性体是一种分子复合物，它通过“白介素-1beta”等“促炎性”细胞因子的成熟来触发先天性免疫防卫，以响应如感染和代谢失调等危险信号。现在，Jürg Tschopp等人报告了线粒体在这个过程中所起的一个出乎意料的中心作用。NLRP3炎性体是被由受损线粒体分泌的活性氧激发的。这项工作表明，线粒体不仅是细胞凋亡所必需的，而且是炎症反应所必需的。（生物谷 Bioon.com）
生物谷推荐原文出处：
Nature doi:10.1038/nature09663
A role for mitochondria in NLRP3 inflammasome activation
Rongbin Zhou,Amir S. Yazdi,Philippe Menu& Jürg Tschopp
An inflammatory response initiated by the NLRP3 inflammasome is triggered by a variety of situations of host ‘danger’, including infection and metabolic dysregulation1, 2. Previous studies suggested that NLRP3 inflammasome activity is negatively regulated by autophagy and positively regulated by reactive oxygen species (ROS) derived from an uncharacterized organelle. Here we show that mitophagy/autophagy blockade leads to the accumulation of damaged, ROS-generating mitochondria, and this in turn activates the NLRP3 inflammasome. Resting NLRP3 localizes to endoplasmic reticulum structures, whereas on inflammasome activation both NLRP3 and its adaptor ASC redistribute to the perinuclear space where they co-localize with endoplasmic reticulum and mitochondria organelle clusters. Notably, both ROS generation and inflammasome activation are suppressed when mitochondrial activity is dysregulated by inhibition of the voltage-dependent anion channel. This indicates that NLRP3 inflammasome senses mitochondrial dysfunction and may explain the frequent association of mitochondrial damage with inflammatory diseases.
