Mitochondria in innate immunity

被引：199

作者：

Arnoult, Damien ^{[2
]}

Soares, Fraser ^{[1
]}

Tattoli, Ivan ^{[1
]}

Girardin, Stephen E. ^{[1
]}

机构：

[1] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON M5S 1A8, Canada

[2] Hop Paul Brousse, INSERM, U1014, F-94807 Villejuif, France

来源：

EMBO REPORTS | 2011年 / 12卷 / 09期

关键词：

mitochondria; innate immunity; MAVS; pathogen; host metabolism; NLRP3 INFLAMMASOME ACTIVATION; NF-KAPPA-B; RIG-I; ADAPTER PROTEIN; RECEPTOR; MAVS; RECOGNITION; AUTOPHAGY; RESPONSES; NLRX1;

D O I：

10.1038/embor.2011.157

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Mitochondria are cellular organelles involved in host-cell metabolic processes and the control of programmed cell death. A direct link between mitochondria and innate immune signalling was first highlighted with the identification of MAVS-a crucial adaptor for RIGI-like receptor signalling-as a mitochondria-anchored protein. Recently, other innate immune molecules, such as NLRX1, TRAF6, NLRP3 and IRGM have been functionally associated with mitochondria. Furthermore, mitochondrial alarmins-such as mitochondrial DNA and formyl peptides-can be released by damaged mitochondria and trigger inflammation. Therefore, mitochondria emerge as a fundamental hub for innate immune signalling.

引用

页码：901 / 910

页数：10