IFN-Inducible SerpinA5 Triggers Antiviral Immunity by Regulating STAT1 Phosphorylation and Nuclear Translocation.
IFN-Inducible SerpinA5 Triggers Antiviral Immunity by Regulating STAT1 Phosphorylation and Nuclear Translocation.
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DOI：
10.3390/ijms24065458
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发表时间：
2023-03-13
影响因子：
5.6
通讯作者：
Sun, Caijun
中科院分区：
文献类型：
--
作者：
Wang, Congcong;Liu, Yajie;Liu, Xinglai;Zhao, Jin;Lang, Bing;Wu, Fan;Wen, Ziyu;Sun, Caijun
深入了解病毒-宿主相互作用是制定有效战略控制频繁出现的传染病的先决条件，这已成为全球公共卫生的严重挑战。I型干扰素（IFN）介导的JAK/STAT信号通路在宿主抗病毒免疫中发挥重要作用，但IFN刺激基因（ISG）的确切调控机制尚不清楚。SerpinA 5作为一种新的ISG，在抗病毒活性中发挥了以前未被认识的作用。SerpinA 5可以上调STAT 1的磷酸化并促进其核转位，从而有效地激活IFN相关信号通路的转录以削弱病毒感染。我们的数据提供了病毒-宿主相互作用期间SerpinA 5介导的先天免疫信号传导的见解。
Deeply understanding virus-host interactions is a prerequisite for developing effective strategies to control frequently emerging infectious diseases, which have become a serious challenge for global public health. The type I interferon (IFN)-mediated JAK/STAT pathway is well known for playing an essential role in host antiviral immunity, but the exact regulatory mechanisms of various IFN-stimulated genes (ISGs) are not yet fully understood. We herein reported that SerpinA5, as a novel ISG, played a previously unrecognized role in antiviral activity. Mechanistically, SerpinA5 can upregulate the phosphorylation of STAT1 and promote its nuclear translocation, thus effectively activating the transcription of IFN-related signaling pathways to impair viral infections. Our data provide insights into SerpinA5-mediated innate immune signaling during virus-host interactions.
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6.7
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