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丙型肝炎病毒通过与Toll样受体7结合来抑制CD4 T细胞功能。

Hepatitis C virus inhibits CD4 T cell function via binding to Toll-like receptor 7.

作者信息

Mele Dalila, Mantovani Stefania, Oliviero Barbara, Grossi Giulia, Ludovisi Serena, Mondelli Mario U, Varchetta Stefania

机构信息

Division of Infectious Diseases and Immunology, Department of Medical Sciences and Infectious Diseases, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.

Internal Medicine and Hepatology Unit, Humanitas Research Hospital, Rozzano, Milan, Italy.

出版信息

Antiviral Res. 2017 Jan;137:108-111. doi: 10.1016/j.antiviral.2016.11.013. Epub 2016 Nov 19.

Abstract

Toll-like receptor 7 (TLR7) is a ssRNA receptor that activates dendritic cells and macrophages upon ssRNA binding; however, little is known of its role in CD4 T cells. We show here that hepatitis C virus (HCV) induces a dose dependent inhibition of cytokine production and expression of activation markers in CD4 T cells, which were restored by a TLR7-specific antagonist. These findings indicate that HCV induces CD4 T cell impairment via TLR7 which may contribute to failure of virus eradication, casting doubts on the use of TLR7 agonists to boost innate immunity in chronic RNA virus infections.

摘要

Toll样受体7(TLR7)是一种单链RNA受体,在与单链RNA结合后可激活树突状细胞和巨噬细胞;然而,其在CD4 T细胞中的作用却鲜为人知。我们在此表明,丙型肝炎病毒(HCV)可诱导CD4 T细胞中细胞因子产生和激活标志物表达的剂量依赖性抑制,而TLR7特异性拮抗剂可恢复这些抑制作用。这些发现表明,HCV通过TLR7诱导CD4 T细胞功能受损,这可能导致病毒清除失败,这也让人对使用TLR7激动剂增强慢性RNA病毒感染中的先天免疫产生怀疑。

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