生物
先天免疫系统
内部收益率3
干扰素
免疫系统
细胞生物学
干扰素调节因子
Ⅰ型干扰素
免疫学
胞浆
体内
病毒学
遗传学
生物化学
酶
作者
Qing Sun,Lijun Sun,Hong-Hsing Liu,Xiang Chen,Rashu B. Seth,James Forman,Zhijian J. Chen
出处
期刊:Immunity
[Elsevier]
日期:2006-05-01
卷期号:24 (5): 633-642
被引量:545
标识
DOI:10.1016/j.immuni.2006.04.004
摘要
The mitochondrial antiviral signaling protein (MAVS) mediates the activation of NFkappaB and IRFs and the induction of interferons in response to viral infection. In vitro studies have also suggested that MAVS is required for interferon induction by cytosolic DNA, but the in vivo evidence is lacking. By generating MAVS-deficient mice, here we show that loss of MAVS abolished viral induction of interferons and prevented the activation of NFkappaB and IRF3 in multiple cell types, except plasmacytoid dendritic cells (pDCs). However, MAVS was not required for interferon induction by cytosolic DNA or by Listeria monocytogenes. Mice lacking MAVS were viable and fertile, but they failed to induce interferons in response to poly(I:C) stimulation and were severely compromised in immune defense against viral infection. These results provide the in vivo evidence that the cytosolic viral signaling pathway through MAVS is specifically required for innate immune responses against viral infection.
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