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

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

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

机译：RIG-I识别RNA病毒可激活CARD9并激活白细胞介素1β产生的炎性体信号传导。

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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.

机译：白细胞介素1 beta（IL-1 beta）是病毒感染期间有效的促炎因子。依赖转录因子NF-κB的Il1b的转录以及随后的炎性小体对前IL-1β的加工，可以严格控制其产生。但是，促进RNA病毒诱导的IL-1β产生的传感器和机制尚未明确定义。在这里，我们报告RNA解旋酶RIG-I在RNA病毒诱导的促炎反应中的双重作用。 RIG-I介导的NF-κB激活需要信号适配器MAVS和适配器CARD9和Bcl-10的复合体，而RIG-I还与适配器ASC结合，通过独立于机制的机制触发caspase-1依赖性炎性体激活。 MAVS，CARD9和Nod样受体蛋白NLRP3的表达。我们的结果确定了CARD9-Bcl-10模块是RIG-I依赖性促炎反应的必要组成部分，并将RIG-I建立为能够响应某些RNA病毒而激活炎性体的传感器。

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《Nature immunology》 |2010年第1期|共7页
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Poeck H; Bscheider M; Gross O; Finger K; Roth S; Rebsamen M; Hannesschlager N; Schlee M; Rothenfusser S; Barchet W; Kato H; Akira S; Inoue S; Endres S; Peschel C; Hartmann G; Hornung V; Ruland J;
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1. Recognition of RNA virus by RIG-I results in activation of CARD9 and inflammasome signaling for interleukin 1 beta production. [J] . Poeck H, Bscheider M, Gross O, Nature immunology . 2010,第1期

机译：RIG-I识别RNA病毒可激活CARD9并激活白细胞介素1β产生的炎性体信号传导。
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3. C and V proteins of Sendai virus target signaling pathways leading to IRF-3 activation for the negative regulation of interferon-beta production. [J] . Komatsu T, Takeuchi K, Yokoo J, Virology . 2004,第1期

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6. Two MicroRNAs Encoded within the Bovine Herpesvirus 1 Latency-Related Gene Promote Cell Survival by Interacting with RIG-I and Stimulating NF-κB-Dependent Transcription and Beta Interferon Signaling Pathways [O] . Leticia Frizzo da Silva, Clinton Jones 2012

机译：牛疱疹病毒1潜伏期相关基因中编码的两个MicroRNA通过与RIG-I相互作用并刺激NF-κB依赖性转录和β干扰素信号传导途径来促进细胞存活。
7. RNA and beta-Hemolysin of Group B Streptococcus Induce Interleukin-1 beta ( IL-1 beta) by Activating NLRP3 Inflammasomes in Mouse Macrophages [O] . Gupta, Rahul, Ghosh, Shubhendu, Monks, Brian, 2014

机译：B组链球菌的RNA和β-溶血素通过激活小鼠巨噬细胞中的NLRP3炎性小体诱导白介素1 beta（IL-1 beta）
8. Activated Human Langerhans Cells Express mRNA for Interleukin-1(alpha) and Interleukin-1(beta) and Produce These Cytokines but do not Secrete Them. [R] . Morhenn, V. B., Lee, S. W., Ilnicka, M., 1989

机译：激活的人朗格汉斯细胞表达白细胞介素-1（α）和白细胞介素-1（β）的mRNa并产生这些细胞因子但不分泌它们。

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

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