期刊
NATURE IMMUNOLOGY
卷 11, 期 1, 页码 63-1824出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1824
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资金
- Bundesministerium fur Bildung und Forschung Biofuture
- Deutsche Forschungsgemeinschaft [SFB704, SFB670, SFB832, KFO177]
- Sonderforschungsbereiche
- Graduiertenkolleg [1202, RO 2525/3-1]
- Center for Integrated Protein Science Munich
- European Research Council
- Deutsche Krebshilfe
Interleukin 1 beta (IL-1 beta) is a potent proinflammatory factor during viral infection. Its production is tightly controlled by transcription of Il1b dependent on the transcription factor NF-kappa B and subsequent processing of pro-IL-1 beta by an inflammasome. However, the sensors and mechanisms that facilitate RNA virus-induced production of IL-1 beta are not well defined. Here we report a dual role for the RNA helicase RIG-I in RNA virus-induced proinflammatory responses. Whereas RIG-I-mediated activation of NF-kappa B required the signaling adaptor MAVS and a complex of the adaptors CARD9 and Bcl-10, RIG-I also bound to the adaptor ASC to trigger caspase-1-dependent inflammasome activation by a mechanism independent of MAVS, CARD9 and the Nod-like receptor protein NLRP3. Our results identify the CARD9-Bcl-10 module as an essential component of the RIG-I-dependent proinflammatory response and establish RIG-I as a sensor able to activate the inflammasome in response to certain RNA viruses.
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