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Interferon Independent Non-Canonical STAT Activation and Virus Induced Inflammation

机译:干扰素依赖性非规范STAT激活和病毒诱导的炎症

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摘要

Interferons (IFNs) are a group of secreted proteins that play critical roles in antiviral immunity, antitumor activity, activation of cytotoxic T cells, and modulation of host immune responses. IFNs are cytokines, and bind receptors on cell surfaces to trigger signal transduction. The major signaling pathway activated by IFNs is the JAK/STAT (Janus kinase/signal transducer and activator of transcription) pathway, a complex pathway involved in both viral and host survival strategies. On the one hand, viruses have evolved strategies to escape from antiviral host defenses evoked by IFN-activated JAK/STAT signaling. On the other hand, viruses have also evolved to exploit the JAK/STAT pathway to evoke activation of certain STATs that somehow promote viral pathogenesis. In this review, recent progress in our understanding of the virus-induced IFN-independent STAT signaling and its potential roles in viral induced inflammation and pathogenesis are summarized in detail, and perspectives are provided.
机译:干扰素(IFN)是一类分泌蛋白,在抗病毒免疫,抗肿瘤活性,细胞毒性T细胞活化和宿主免疫应答调节中起关键作用。 IFN是细胞因子,与细胞表面的受体结合以触发信号转导。 IFN激活的主要信号传导途径是JAK / STAT(Janus激酶/信号转导和转录激活剂)途径,这是一种涉及病毒和宿主生存策略的复杂途径。一方面,病毒已发展出逃避由IFN激活的JAK / STAT信号转导引起的抗病毒宿主防御的策略。另一方面,病毒也已经进化以利用JAK / STAT途径来激发某些以某种方式促进病毒发病机理的STAT的激活。在这篇综述中,我们对病毒诱导的独立于IFN的STAT信号及其在病毒诱导的炎症和发病机制中的潜在作用的理解的最新进展得到了详细总结,并提供了一些见解。

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