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SNW1 interacts with IKKγ to positively regulate antiviral innate immune responses against influenza A virus infection.
Microbes and Infection ( IF 5.8 ) Pub Date : 2020-08-14 , DOI: 10.1016/j.micinf.2020.07.009
Qiao Zhang 1 , Taizhen Liang 1 , Shuyin Gu 1 , Yilu Ye 1 , Shuwen Liu 2
Affiliation  

The Ski-interacting protein (SNW1) acts as a transcriptional co-regulator associated with mRNA splicing and transcription, cell cycle progression, acute and chronic inflammatory responses, however, its role involved in host antiviral innate immune responses remains to be explored. Here, for the first time, we demonstrated that SNW1 positively regulates the expression of pro-inflammatory cytokines and interferon (IFN) responses induced by influenza A virus (IAV) infection, and further inhibits virus replication by performing SNW1 depletion or overexpression approaches. Furthermore, we showed that reduced interferon beta (IFN-β) expression caused by interfering SNW1 impairs the activation of JAK-STAT pathway in response to IAV or poly I:C. Importantly, by interacting with IKKγ, the regulatory subunit of IκB kinase (IKK) complex, SNW1 promotes IAV-induced activation of NF-κB and phosphorylation of TBK1 kinase, leading to the increase of antiviral effectors interleukin 6 (IL-6), C-X-C motif chemokine 10 (CXCL10), IFN-β and myxovirus resistance protein 1 (MX1). Taken together, our study revealed that SNW1 is an important mediator of host defenses against IAV through the induction of pro-inflammatory factors and IFN signaling, providing novel insights in modulating innate immune responses to protect host from IAV infection.



中文翻译:

SNW1与IKKγ相互作用以积极调节针对A型流感病毒感染的抗病毒先天免疫应答。

滑雪相互作用蛋白(SNW1)作为与mRNA剪接和转录,细胞周期进程,急性和慢性炎症反应相关的转录共调节因子,但是,其在宿主抗病毒先天免疫反应中的作用尚待探索。在这里,我们首次证明SNW1积极调节甲型流感病毒(IAV)感染诱导的促炎性细胞因子和干扰素(IFN)反应的表达,并通过执行SNW1耗竭或过表达方法进一步抑制病毒复制。此外,我们表明,由干扰SNW1引起的干扰素β(IFN-β)表达降低会削弱JAK-STAT途径对IAV或poly I:C的响应。重要的是,通过与IKKB激酶(IKK)复合体的调节亚基IKKγ相互作用,SNW1促进IAV诱导的NF-κB活化和TBK1激酶的磷酸化,从而导致抗病毒效应因子白介素6(IL-6),CXC基序趋化因子10(CXCL10),IFN-β和粘液病毒抗性蛋白1(MX1)的增加。 。两者合计,我们的研究表明SNW1通过诱导促炎因子和IFN信号传导,是宿主抵抗IAV的重要介体,为调节先天免疫应答以保护宿主免受IAV感染提供了新的见解。

更新日期:2020-08-14
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