期刊
CELL HOST & MICROBE
卷 8, 期 6, 页码 496-509出版社
CELL PRESS
DOI: 10.1016/j.chom.2010.11.008
关键词
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资金
- Mitsubishi Foundation
- Mochida Foundation
- Akiyama Life Science Foundation
- Ministry of Education, Science, and Culture
- Ministry of Health, Labor, and Welfare of Japan
- Grants-in-Aid for Scientific Research [21687018, 22790450] Funding Source: KAKEN
RNA virus infection is recognized by the RIG-I-like receptors RIG-I and MDA5, which induce antiviral responses including the production of type I interferons (IFNs) and proinflammatory cytokines. RIG-I is regulated by Lys63-linked polyubiquitination, and three E3 ubiquitin ligases, RNF125, TRIM25, and Rip let, are reported to target RIG-I for ubiquitination. To examine the importance of Rip let in vivo, we generated Rip let-deficient mice. Fibroblasts, macrophages, and conventional dendritic cells from Riplet-deficient animals were defective for the production of IFN and other cytokines in response to infection with several RNA viruses. However, Rip let was dispensable for the production of IFN in response to B-DNA and DNA virus infection. Rip let deficiency abolished RIG-I activation during RNA virus infection, and the mutant mice were more susceptible to vesicular stomatitis virus infection than wild-type mice. These data indicate that Rip let is essential for regulating RIG-I-mediated innate immune response against RNA virus infection in vivo.
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