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Recognition of RNA virus by RIG-I results in activation of CARD9 and inflammasome signaling for interleukin 1β production

Authors :
Veit Hornung
Shizuo Akira
Susanne Roth
Simon Rothenfusser
Martin Schlee
Hiroki Kato
Satoshi Inoue
Manuele Rebsamen
Katrin Finger
Hendrik Poeck
Nicole Hannesschläger
Jürgen Ruland
Winfried Barchet
Christian Peschel
Stefan Endres
Michael Bscheider
Gunther Hartmann
Olaf Gross
Source :
Nature Immunology. 11:63-69
Publication Year :
2009
Publisher :
Springer Science and Business Media LLC, 2009.

Abstract

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-kappaB 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-kappaB 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.

Details

ISSN :
15292916 and 15292908
Volume :
11
Database :
OpenAIRE
Journal :
Nature Immunology
Accession number :
edsair.doi.dedup.....572e2f8686d95f1909922dce333f6b7e
Full Text :
https://doi.org/10.1038/ni.1824