期刊
ISCIENCE
卷 25, 期 7, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.isci.2022.104599
关键词
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资金
- AgenceNationale de Recherches sur le SIDA et les hepatites virales 2012-1 and 2012-2 HIV signature on RIG-I-like receptors
- Agence Nationale pour la Recherche [ANR-16CE15-0025-01]
- Fondation pour la Recherche Medicale [FDT20140931129]
- National Institutes of Health [R01CA201189, R01CA180913, R01AI081848, U01CA228963, R01CA240924, P30CA008748]
- Stand Up To Cancer-National Science Foundation-Lustgarten Foundation Convergence Dream Team Grant - Stand Up to Cancer
- Lustgarten Foundation
- V Foundation
- National Science Foundation [NSF 1545935]
- Mark Foundation for Cancer Research
- Bristol-Meyers Squibb
- Cancer Research Institute
- Merck
- Regeneron
- Ludwig Institute
- Melanoma Research Alliance
- Leukemia & Lymphoma Society
- Antidote Health Foundation
This study reveals the role of endogenous RNA in antiviral immunity, particularly in interaction with RLRs during different types of RNA virus infections. Specific endogenous RNAs bind to RLRs and induce immune response, indicating the importance of endogenous ligands in PRR activation.
Pattern recognition receptors (PRRs) protect against microbial invasion by de-tecting specific molecular patterns found in pathogens and initiating an immune response. Although microbial-derived PRR ligands have been extensively charac-terized, the contribution and relevance of endogenous ligands to PRR activation remains overlooked. Here, we characterize the landscape of endogenous ligands that engage RIG-I-like receptors (RLRs) upon infection by different RNA viruses. In each infection, several RNAs transcribed by RNA polymerase III (Pol3) specif-ically engaged RLRs, particularly the family of Y RNAs. Sensing of Y RNAs was dependent on their mimicking of viral secondary structure and their 5'-triphos-phate extremity. Further, we found that HIV-1 triggered a VPR-dependent down -regulation of RNA triphosphatase DUSP11 in vitro and in vivo, inducing a tran-scriptome-wide change of cellular RNA 5'-triphosphorylation that licenses Y RNA immunogenicity. Overall, our work uncovers the contribution of endoge-nous RNAs to antiviral immunity and demonstrates the importance of this pathway in HIV-1 infection.
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