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

Autor: Poeck, Hendrik, Bscheider, Michael, Gross, Olaf, Finger, Katrin, Roth, Susanne, Rebsamen, Manuele, Hannesschläger, Nicole, Schlee, Martin, Rothenfusser, Simon, Barchet, Winfried, Kato, Hiroki, Akira, Shizuo, Inoue, Satoshi, Endres, Stefan, Peschel, Christian, Hartmann, Gunther, Hornung, Veit, Ruland, Jürgen
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Zdroj: Nature Immunology; Jan2010, Vol. 11 Issue 1, p63-69, 7p, 7 Graphs
Abstrakt: 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-κB 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-κB 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. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index