内部收益率3
磷酸化
生物
安普克
细胞生物学
病毒
蛋白激酶A
干扰素
信号转导
信号转导衔接蛋白
病毒学
坦克结合激酶1
先天免疫系统
免疫系统
免疫学
丝裂原活化蛋白激酶激酶
作者
Cheng Qin,Chunxiao Niu,Zhuo Shen,Yaolin Zhang,Genyu Liu,Chunmei Hou,Jing Dong,Min Zhao,Qianqian Cheng,Xinglun Yang,Jiyan Zhang
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:2021-09-01
卷期号:207 (5): 1411-1418
被引量:5
标识
DOI:10.4049/jimmunol.2100086
摘要
Abstract The receptor for activated C kinase 1 (RACK1) adaptor protein has been implicated in viral infection. However, whether RACK1 promotes in vivo viral infection in mammals remains unknown. Moreover, it remains elusive how RACK1 is engaged in antiviral innate immune signaling. In this study, we report that myeloid RACK1 deficiency does not affect the development and survival of myeloid cells under resting conditions but renders mice less susceptible to viral infection. RACK1-deficient macrophages produce more IFN-α and IFN-β in response to both RNA and DNA virus infection. In line with this, RACK1 suppresses transcriptional activation of type 1 IFN gene promoters in response to virus infection. Analysis of virus-mediated signaling indicates that RACK1 inhibits the phosphorylation of IRF3/7. Indeed, RACK1 interacts with IRF3/7, which is enhanced after virus infection. Further exploration indicates that virus infection triggers AMPK activation, which in turn phosphorylates RACK1 at Thr50. RACK1 phosphorylation at Thr50 enhances its interaction with IRF3/7 and thereby limits IRF3/7 phosphorylation. Thus, our results confirm that myeloid RACK1 promotes in vivo viral infection and provide insight into the control of type 1 IFN production in response to virus infection.
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