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

Hendrik Poeck, Michael Bscheider, Olaf Gross, Katrin Finger, Susanne Roth, Manuele Rebsamen, Nicole Hannesschläger, Martin Schlee, Simon Rothenfusser, Winfried Barchet, Hiroki Kato, Shizuo Akira, Satoshi Inoue, Stefan Endres, Christian Peschel, Gunther Hartmann, Veit Hornung, Jürgen Ruland

Research output: Contribution to journalArticlepeer-review

435 Scopus citations

Abstract

Interleukin 1Β (IL-1Β) is a potent proinflammatory factor during viral infection. Its production is tightly controlled by transcription of Il1b dependent on the transcription factor NF-B and subsequent processing of pro-IL-1Β by an inflammasome. However, the sensors and mechanisms that facilitate RNA virus-induced production of IL-1Β 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-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.

Original languageEnglish
Pages (from-to)63-69
Number of pages7
JournalNature Immunology
Volume11
Issue number1
DOIs
StatePublished - Jan 2010
Externally publishedYes

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