Regulation of antiviral innate immune responses by RIG-I family of RNA helicases

被引:0
|
作者
Onomoto, K. [1 ,2 ]
Yoneyama, M. [1 ,2 ]
Fujita, T. [1 ,2 ]
机构
[1] Kyoto Univ, Inst Virus Res, Mol Genet Lab, Kyoto 606, Japan
[2] Kyoto Univ, Grad Sch Biostudies, Mol Cell Biol Lab, Kyoto 606, Japan
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暂无
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The recognition of viral nucleic acids with pattern recognition receptors (PRRs) is the first step in inducing the innate immune system. Type I interferons (IFNs), central mediators in antiviral innate immunity, along with other cytokines and chemokines, disrupt virus replication. Recent studies indicated at least two distinct pathways for the induction of type I IFN by viral infection. Toll-like receptors (TLRs) are extracellular or endosomal PRRs for microbial pathogens, whereas retinoic acid-inducible gene-I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5) are novel intracellular PRRs for the viral dsRNA. In this review, we describe the distinct mechanisms inducing type I IFNs through TLRs and RIG-I/MDA5 pathways.
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页码:193 / 205
页数:13
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