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MicroRNA-218 通过靶向 RIG-I 抑制 I 型干扰素的产生并促进病毒免疫逃逸。

MicroRNA-218 inhibits type I interferon production and facilitates virus immune evasion via targeting RIG-I.

机构信息

Department of Stomatology, Fourth Affiliated Hospital, Hebei Medical University, Shijiazhuang, Hebei, China.

Department of Pathology, Chinese Medicine Hospital in Hebei Province, Shijiazhuang, Hebei, China.

出版信息

Biotechnol Appl Biochem. 2020 May;67(3):396-403. doi: 10.1002/bab.1882. Epub 2020 Jan 15.

Abstract

The host protective immunity against viral infection requires the effective detection of viral antigens and the subsequent production of type I interferons (IFNs) by host immune cells. Retinoic acid-inducible gene I (RIG-I) is the crucial signaling element responsible for sensing viral RNA component and initiating the downstream antiviral signaling pathways, leading to the production of type I IFNs. In this work, we identified microRNA-218 (miR-218) as a new virus-induced miRNA that dampens the expression of RIG-I in mouse and human macrophages, leading to the impaired production of type I IFNs. Interfering miR-218 expression rescued RIG-I-mediated antiviral signaling and thus protected macrophages from viral infection. Hence, our results provide new understanding of miRNA-mediated viral immune evasion and may be potentially useful for the treatment of viral infection in the future.

摘要

宿主对病毒感染的保护性免疫需要宿主免疫细胞有效检测病毒抗原,并随后产生 I 型干扰素 (IFNs)。视黄酸诱导基因 I (RIG-I) 是负责检测病毒 RNA 成分并启动下游抗病毒信号通路的关键信号元件,导致 I 型 IFNs 的产生。在这项工作中,我们鉴定了 microRNA-218 (miR-218) 作为一种新的病毒诱导的 microRNA,可下调小鼠和人巨噬细胞中 RIG-I 的表达,导致 I 型 IFNs 的产生受损。干扰 miR-218 的表达挽救了 RIG-I 介导的抗病毒信号,从而保护巨噬细胞免受病毒感染。因此,我们的研究结果提供了对 microRNA 介导的病毒免疫逃避的新认识,将来可能对病毒感染的治疗有用。

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