The Cross-Regulation Between Autophagy and Type I Interferon Signaling in Host Defense
The Cross-Regulation Between Autophagy and Type I Interferon Signaling in Host Defense
复制标题
宿主防御中自噬和 I 型干扰素信号传导之间的交叉调节。
DOI：
10.1007/978-981-15-0606-2_8
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发表时间：
2019-01-01
期刊：
影响因子：
--
通讯作者：
Jin, Shouheng
中科院分区：
文献类型：
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作者：
Jin, Shouheng
I型干扰素（IFN）的产生是细胞内抗菌程序的标志之一。典型的I型干扰素应答激活Janus激酶（JAK）-信号转导子和转录激活子（STAT）途径，导致大量干扰素刺激基因（ISG）转录，从而建立全面的抗病毒状态。I型IFN信号应及时启动，以激发先天性和适应性免疫应答，从而有效地消除入侵病原体。同时，必须进行精确的控制以抑制I型IFN应答的持续激活，以避免伴随的毒性。自噬是一种保守的真核生物降解系统，由许多自噬相关蛋白（autophagy-related protein，ATG）介导，在清除入侵微生物和操纵I型反应中起着重要作用。自噬通过与先天免疫信号传导途径的调节整合以及通过去除先天免疫传感器的内源性配体来调节I型IFN应答。此外，选择性自噬支配选择先天免疫因子作为降解的特异性货物，从而密切监测I型IFN应答。本文就自噬与I型干扰素信号在宿主防御中的交叉调节作用作一综述。
The production of type I interferons (IFNs) is one of the hallmarks of intracellular antimicrobial program. Typical type I IFN response activates the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway, which results in the transcription of plentiful IFN-stimulated genes (ISGs) to establish the comprehensive antiviral states. Type I IFN signaling should initiate timely to provoke innate and adaptive immune responses for effective elimination of the invading pathogens. Meanwhile, a precise control must come on the stage to restrain the persistent activation of type I IFN responses to avoid attendant toxicity. Autophagy, a conserved eukaryotic degradation system, mediated by a number of autophagy-related (ATG) proteins, plays an essential role in the clearance of invading microorganism and manipulation of type I responses. Autophagy modulates type I IFN responses through regulatory integration with innate immune signaling pathways, and by removing endogenous ligands of innate immune sensors. Moreover, selective autophagy governs the choice of innate immune factors as specific cargoes for degradation, thus tightly monitoring the type I IFN responses. This review will focus on the cross-regulation between autophagy and type I IFN signaling in host defense.