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Poeck, H.* ; Bscheider, M.* ; Gross, O.* ; Finger, K.* ; Roth, S. ; Rebsamen, M.* ; Hannesschläger, N.* ; Schlee, M.* ; Rothenfusser, S.* ; Barchet, W.* ; Kato, H.* ; Akira, S.* ; Inoue, S.* ; Endres, S.* ; Peschel, C.* ; Hartmann, G.* ; Hornung, V.* ; Ruland, J.

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

Nat. Immunol. 11, 63-69 (2010)
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter nf-kappa-b; double-stranded-rna; innate immune-responses; adapter protein card9; toll-like receptor; nlrp3 inflammasome; cytoplasmic dna; cutting edge; antiviral responses; 5'-triphosphate rna
ISSN (print) / ISBN 1529-2908
e-ISSN 1529-2916
Zeitschrift Nature Immunology
Quellenangaben Band: 11, Heft: 1, Seiten: 63-69 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Begutachtungsstatus Peer reviewed