RIG-I-like receptors: cytoplasmic sensors for non-self RNA

被引:267
作者
Kato, Hiroki [2 ]
Takahasi, Kiyohiro [3 ]
Fujita, Takashi [1 ,2 ]
机构
[1] Kyoto Univ, Inst Virus Res, Mol Genet Lab, Sakyo Ku, Kyoto 6068507, Japan
[2] Kyoto Univ, Grad Sch Biostudies, Mol Cell Biol Lab, Kyoto 6068507, Japan
[3] Kyoto Univ, Grad Sch Pharmaceut Sci, Inst Innovat NanoBio Drug Discovery & Dev, Kyoto 6068507, Japan
关键词
antiviral innate immunity; type I interferon; RIG-I-like receptors; non-self RNA; DOUBLE-STRANDED-RNA; HEPATITIS-C VIRUS; INDUCIBLE GENE-I; ANTIVIRAL IMMUNE-RESPONSES; E3 UBIQUITIN LIGASE; NF-KAPPA-B; INNATE IMMUNITY; INTERFERON INDUCTION; PATTERN-RECOGNITION; NEGATIVE REGULATION;
D O I
10.1111/j.1600-065X.2011.01052.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Viral infection results in the generation of non-self RNA species in the cells, which is recognized by retinoic acid inducible gene-I-like receptors (RLRs), and initiates innate antiviral responses, including the production of proinflammatory cytokines and type I interferon. In this review, we summarize reports on virus-specificity of RLRs, structures of non-self RNA patterns, structural biology of RLRs, and the signaling adapter molecules involved in antiviral innate immunity.
引用
收藏
页码:91 / 98
页数:8
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