Intercellular Communication Is Key for Protective IFN/ Signaling During Viral Central Nervous System Infection
Intercellular Communication Is Key for Protective IFN/ Signaling During Viral Central Nervous System Infection
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DOI：
10.1089/vim.2018.0101
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发表时间：
2018-09-15
期刊：
影响因子：
2.2
通讯作者：
Bergmann, Cornelia C.
中科院分区：
文献类型：
--
作者：
Hwang, Mihyun;Bergmann, Cornelia C.
多种病毒可引起中枢神经系统（CNS）感染和神经系统疾病，虽然发病率很低。与外周感染类似，IFN/γ诱导和信号传导构成了限制病毒传播的第一道防线。然而，CNS驻留细胞在IFN/途径中的基础和诱导组分的库和幅度方面存在很大差异。虽然小胶质细胞作为常驻骨髓细胞已经被认为是CNS入侵病原体或损伤的突出哨兵，但星形胶质细胞正在成为许多嗜神经RNA病毒感染的关键应答者。以RNA病毒为重点，本文综述了星形胶质细胞作为IFN/诱导剂和应答者的作用，并探讨了IFN/受体信号在调节骨髓细胞活化和IFN应答中的作用。一个概括的图片出现牵连IFN/不仅作为关键建立经典的抗病毒状态，但也协调细胞的流动性和IFN介导的效应功能。
A variety of viruses can induce central nervous system (CNS) infections and neurological diseases, although the incidence is rare. Similar to peripheral infections, IFN/ induction and signaling constitutes a first line of defense to limit virus dissemination. However, CNS-resident cells differ widely in their repertoire and magnitude of both basal and inducible components in the IFN/ pathway. While microglia as resident myeloid cells have been implicated as prominent sentinels of CNS invading pathogens or insults, astrocytes are emerging as key responders to many neurotropic RNA virus infections. Focusing on RNA viruses, this review discusses the role of astrocytes as IFN/ inducers and responders and touches on the role of IFN/ receptor signaling in regulating myeloid cell activation and IFN responsiveness. A summary picture emerges implicating IFN/ not only as key in establishing the classical antiviral state, but also orchestrating cell mobility and IFN-mediated effector functions.