Vimentin inhibits type I interferon production by disrupting the TBK1-IKK epsilon-IRF3 axis
文献类型： 外文期刊
作者： Liu, Hongyang 1 ; Ye, Guangqiang 1 ; Liu, Xiaohong 1 ; Xue, Mengdi 1 ; Zhou, Qiongqiong 1 ; Zhang, Longfeng 1 ; Zhang, Kunli 3 ; Huang, Li 1 ; Weng, Changjiang 1 ;
作者机构： 1.Chinese Acad Agr Sci, Div Fundamental Immunol, State Key Lab Vet Biotechnol, Harbin Vet Res Inst, Harbin 150069, Peoples R China
2.Heilongjiang Prov Key Lab Vet Immunol, Harbin 150069, Peoples R China
3.Guangdong Acad Agr Sci, Inst Anim Hlth, Guangzhou 510640, Peoples R China
期刊名称：CELL REPORTS （ 影响因子：9.995； 五年影响因子：10.99 ）
ISSN： 2211-1247
年卷期： 2022 年 41 卷 2 期
页码：
收录情况： SCI
摘要： Cytoskeleton proteins have been reported to be involved in the host antiviral immune responses. However, how cytoskeleton proteins regulate host antiviral immune responses is not fully understood. Here we report that the cytoskeletal protein vimentin is a negative regulator of type I interferon (IFN-I) production upon viral infection. Ectopic expression of vimentin suppresses RNA-and DNA viruses-induced IFN-I production, whereas knockout of vimentin expression enhances IFN-I production. Viral infection increases vimentin expression and ultimately inhibits IFN-I production. Mechanistically, upregulated vimentin interacts with TBK1 and IKK epsilon to disrupt the interactions of TBK1-IRF3 and IKK epsilon-IRF3, resulting in inhibition of IRF3 phos-phorylation and nuclear translocation. Furthermore, we generate vimentin knockout mice to confirm that defi-ciency of vimentin gene in mice suppressed encephalomyocarditis virus replication in vivo. Our findings dem-onstrates that vimentin plays an important role in regulating IFN-I production, revealing its antiviral function of the cytoskeletal protein vimentin.
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