Regulation of antiviral innate immune responses by RIG-I family of RNA helicases.
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.
Onomoto
K
K
Laboratory of Molecular Genetics, Institute for Virus Research, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.
Yoneyama
M
M
Fujita
T
T
D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D007370:Interferon Type I / Q000276:immunology*; D000072640:Interferon-Induced Helicase, IFIH1; D011971:Receptors, Immunologic; D051193:Toll-Like Receptors / Q000276:immunology; D014777:Virus Diseases / Q000276:immunology*
D007370:Interferon Type I; D011971:Receptors, Immunologic; D051193:Toll-Like Receptors; C452820:RIGI protein, human; C452815:IFIH1 protein, human; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases; D000072640:Interferon-Induced Helicase, IFIH1