"Toll-free" pathways for production of type I interferons.
"Toll-free" pathways for production of type I interferons.
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DOI：
10.3934/allergy.2017.3.143
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发表时间：
2017
影响因子：
0.7
通讯作者：
Ning S
中科院分区：
文献类型：
--
作者：
Wang L;Ning S
病原体相关分子模式（PAMPs）和损伤相关分子模式（DAMPs）由不同的细胞病原体识别受体（PRRs）识别，PRRs表达于先天免疫系统细胞的细胞膜或细胞质中。来源于病原体或某些细胞条件的核酸代表了一大类PAMP/DAMP，其通过特异性结合细胞内Toll样受体或胞质受体而触发除促炎细胞因子之外的I型干扰素（IFN-I）的产生。这些胞质受体与TLR无关，我们称之为“Toll-free”受体，包括RNA敏感RIG-I样受体（RLR）、DNA敏感HIN 200家族和cGAS等。病毒已经进化出无数的策略来唤起宿主细胞和病毒因子以逃避IFN-1介导的先天免疫应答，以促进它们的感染、复制和潜伏期的建立。本文综述了这些“免费”的先天免疫途径及其调控的最新进展，重点关注具有酶活性的细胞和病毒因子。
Pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) are recognized by different cellular pathogen recognition receptors (PRRs), which are expressed on cell membrane or in the cytoplasm of cells of the innate immune system. Nucleic acids derived from pathogens or from certain cellular conditions represent a large category of PAMPs/DAMPs that trigger production of type I interferons (IFN-I) in addition to pro-inflammatory cytokines, by specifically binding to intracellular Toll-like receptors or cytosolic receptors. These cytosolic receptors, which are not related to TLRs and we call them “Toll-free” receptors, include the RNA-sensing RIG-I like receptors (RLRs), the DNA-sensing HIN200 family, and cGAS, amongst others. Viruses have evolved myriad strategies to evoke both host cellular and viral factors to evade IFN-I-mediated innate immune responses, to facilitate their infection, replication, and establishment of latency. This review outlines these “Toll-free” innate immune pathways and recent updates on their regulation, with focus on cellular and viral factors with enzyme activities.