Inhibition of RIG-I and MDA5-dependent antiviral response by gC1qR at mitochondria

被引：108

作者：

Xu, Lijuan ^{[1
]}

Xiao, Nengming ^{[1
]}

Liu, Feng ^{[1
]}

Ren, Hongwei ^{[1
]}

Gu, Jun ^{[1
]}

机构：

[1] Peking Univ, Natl Key Lab Prot Engn & Plant Gene Engn, Coll Life Sci, Beijing 100871, Peoples R China

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2009年 / 106卷 / 05期

基金：

美国国家科学基金会;

关键词：

innate immunity; RIG-I signaling; virus; DOUBLE-STRANDED-RNA; HEPATITIS-C VIRUS; NEGATIVE REGULATION; ADAPTER PROTEIN; INNATE IMMUNITY; BINDING-PROTEIN; RECEPTOR; P-32; ACTIVATION; IDENTIFICATION;

D O I：

10.1073/pnas.0811029106

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

gC1qR is one of the C1q receptors implicated in the regulation of innate and adaptive immunity. We found that gC1qR inhibits RIG-I and MDA5-dependent antiviral signaling. Double stranded RNA and virus trigger the translocation of gC1qR to the mitochondrial outer membrane leading to the interaction of gC1qR with the RIG-I and MDA5 adaptor, VISA/MAVS/IPS-1/Cardif. The interaction of gC1qR with VISA/MAVS/IPS-1/Cardif at mitochondria results in the disruption of RIG-I and MDA5 signaling and the promotion of virus replication. Knockdown of endogenous gC1qR enhances RIG-I-dependent antiviral signaling, and augments the inhibition of virus proliferation. Therefore, gC1qR is a physiological inhibitor of the RIG-I and MDA5-mediated antiviral signaling pathway. These data uncover a new viral mechanism used to negatively control antiviral signaling in host cells.

引用

页码：1530 / 1535

页数：6

共 33 条

[1] Pathogen recognition and innate immunity [J].