NLRP3炎性體是一種分子復(fù)合物,，它通過“白介素-1beta”等“促炎性”細胞因子的成熟來觸發(fā)先天性免疫防衛(wèi)，以響應(yīng)如感染和代謝失調(diào)等危險信號?，F(xiàn)在，Jürg Tschopp等人報告了線粒體在這個過程中所起的一個出乎意料的中心作用,。NLRP3炎性體是被由受損線粒體分泌的活性氧激發(fā)的,。這項工作表明，線粒體不僅是細胞凋亡所必需的,，而且是炎癥反應(yīng)所必需的,。（生物谷 Bioon.com）
生物谷推薦原文出處：
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.
