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Recognition of RNA virus by RIG-I results in activation of CARD9 and inflammasome signaling for interleukin 1 beta production.
Nat Immunol ; 11(1): 63-9, 2010 Jan.
Article em En | MEDLINE | ID: mdl-19915568
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.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Vírus de RNA / Transdução de Sinais / Proteínas Adaptadoras de Transdução de Sinal / RNA Helicases DEAD-box / Interleucina-1beta / Inflamação Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Revista: Nat Immunol Assunto da revista: ALERGIA E IMUNOLOGIA Ano de publicação: 2010 Tipo de documento: Article País de afiliação: Alemanha

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Vírus de RNA / Transdução de Sinais / Proteínas Adaptadoras de Transdução de Sinal / RNA Helicases DEAD-box / Interleucina-1beta / Inflamação Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Revista: Nat Immunol Assunto da revista: ALERGIA E IMUNOLOGIA Ano de publicação: 2010 Tipo de documento: Article País de afiliação: Alemanha