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从病毒到炎症:RIG-I 诱导的 IL-1β 产生的机制。

From virus to inflammation: mechanisms of RIG-I-induced IL-1β production.

机构信息

III. Medizinische Klinik, Klinikum rechts der Isar, Technische Universität München, Munich, Germany.

出版信息

Eur J Cell Biol. 2012 Jan;91(1):59-64. doi: 10.1016/j.ejcb.2011.01.013. Epub 2011 Apr 9.

DOI:10.1016/j.ejcb.2011.01.013
PMID:21481488
Abstract

Early detection of viruses by the innate immune system is critical for host defense. Antiviral immunity is initiated by germline encoded pattern recognition receptors (PRRs) that recognize viral pathogen-associated molecular patterns (PAMPs) such as nucleic acids. Intracellular PRRs then drive the production of interferons and cytokines to orchestrate immune responses. One key host factor that is critical for antiviral immunity and for systemic inflammatory reactions including fever is interleukin-1beta (IL-1β). Here we discuss current insights into the molecular mechanisms how the cytosolic RNA helicase RIG-I triggers NF-κB signaling and inflammasome activation specifically for RNA virus-induced IL-1β production.

摘要

先天免疫系统对病毒的早期检测对于宿主防御至关重要。抗病毒免疫是由识别病毒病原体相关分子模式(PAMPs)(如核酸)的种系编码的模式识别受体(PRRs)启动的。细胞内 PRRs 然后驱动干扰素和细胞因子的产生,以协调免疫反应。一种对抗病毒免疫和包括发热在内的全身炎症反应至关重要的关键宿主因子是白细胞介素-1β(IL-1β)。在这里,我们讨论了细胞质 RNA 解旋酶 RIG-I 如何触发 NF-κB 信号转导和炎性小体激活的分子机制,专门用于 RNA 病毒诱导的 IL-1β 产生。

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