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

被引：428

作者：

Poeck, Hendrik ^{[1
,2
,3
,4
]}

Bscheider, Michael ^{[3
,4
]}

Gross, Olaf ^{[1
]}

Finger, Katrin ^{[1
]}

Roth, Susanne ^{[1
,5
]}

Rebsamen, Manuele ^{[6
]}

Hannesschlaeger, Nicole ^{[1
]}

Schlee, Martin ^{[2
]}

Rothenfusser, Simon ^{[3
,4
]}

Barchet, Winfried ^{[2
]}

Kato, Hiroki ^{[7
]}

Akira, Shizuo ^{[7
]}

Inoue, Satoshi ^{[8
,9
]}

Endres, Stefan ^{[3
,4
]}

Peschel, Christian ^{[1
]}

Hartmann, Gunther ^{[2
]}

Hornung, Veit ^{[2
]}

Ruland, Juergen ^{[1
,5
]}

机构：

[1] Tech Univ Munich, Klinikum Rechts Isar, Med Klin 3, D-8000 Munich, Germany

[2] Univ Klinikum Bonn, Inst Clin Chem & Pharmacol, Bonn, Germany

[3] Univ Munich, Ctr Integrated Prot Sci Munich, Munich, Germany

[4] Univ Munich, Div Clin Pharmacol, Dept Internal Med, Munich, Germany

[5] Res Ctr Environm Hlth, Helmholtz Zentrum Munchen Germany, Lab Signaling Immune Syst, Neuherberg, Germany

[6] Univ Lausanne, Dept Biochem, CH-1066 Epalinges, Switzerland

[7] Osaka Univ, Microbial Dis Res Inst, Dept Host Def, Suita, Osaka 565, Japan

[8] Univ Tokyo, Grad Sch Med, Dept Geriatr Med, Tokyo, Japan

[9] Saitama Med Sch, Res Ctr Genom Med, Saitama, Japan

来源：

NATURE IMMUNOLOGY | 2010年 / 11卷 / 01期

基金：

欧洲研究理事会;

关键词：

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;

D O I：

10.1038/ni.1824

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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-kappa B 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-kappa 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.

引用

页码：63 / 1824

页数：8

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