| Literature DB >> 28916264 |
Tan A Nguyen1, Blake R C Smith2, Michelle D Tate3, Gabrielle T Belz1, Marilou H Barrios1, Kirstin D Elgass4, Alexandra S Weisman5, Paul J Baker1, Simon P Preston1, Lachlan Whitehead1, Alexandra Garnham1, Rachel J Lundie6, Gordon K Smyth7, Marc Pellegrini1, Meredith O'Keeffe6, Ian P Wicks1, Seth L Masters1, Craig P Hunter5, Ken C Pang8.
Abstract
Double-stranded RNA (dsRNA) is a common by-product of viral infections and acts as a potent trigger of antiviral immunity. In the nematode C. elegans, sid-1 encodes a dsRNA transporter that is highly conserved throughout animal evolution, but the physiological role of SID-1 and its orthologs remains unclear. Here, we show that the mammalian SID-1 ortholog, SIDT2, is required to transport internalized extracellular dsRNA from endocytic compartments into the cytoplasm for immune activation. Sidt2-deficient mice exposed to extracellular dsRNA, encephalomyocarditis virus (EMCV), and herpes simplex virus 1 (HSV-1) show impaired production of antiviral cytokines and-in the case of EMCV and HSV-1-reduced survival. Thus, SIDT2 has retained the dsRNA transport activity of its C. elegans ortholog, and this transport is important for antiviral immunity.Entities:
Keywords: EMCV; HSV; MAVS; SIDT2; bystander immunity; double-stranded RNA; type I interferon; virus infection
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Year: 2017 PMID： 28916264 PMCID： PMC5679266 DOI： 10.1016/j.immuni.2017.08.007
Source DB: PubMed Journal: Immunity ISSN： 1074-7613 Impact factor: 31.745