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TLR3 及其信号传导成分的功能失效导致单纯疱疹脑炎。

Functional failure of TLR3 and its signaling components contribute to herpes simplex encephalitis.

机构信息

Division of Immunology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences, Ciszewskiego 8 Str., 02-786 Warsaw, Poland.

Division of Immunology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences, Ciszewskiego 8 Str., 02-786 Warsaw, Poland.

出版信息

J Neuroimmunol. 2018 Mar 15;316:65-73. doi: 10.1016/j.jneuroim.2017.12.011. Epub 2017 Dec 18.

DOI:10.1016/j.jneuroim.2017.12.011
PMID:29305044
Abstract

Herpes simplex encephalitis (HSE) is a severe neurological disease in children and adults caused by herpes simplex virus. This review discusses recent findings on the role of Toll-like receptor 3 (TLR3) deficiencies in the HSE development. Critical checkpoints in the TLR3 signaling that contribute to innate response are discussed, including the importance of TLR3 ligand recognition site and transportation in the cell. We also indicate unresolved issues in the TLR3 functioning that might lead to thorough understanding of immunity during HSE. Such a knowledge base will lead to discovery and design of a rationale therapeutic and preventive approach against HSE.

摘要

单纯疱疹脑炎(HSE)是一种由单纯疱疹病毒引起的儿童和成人严重的神经疾病。本综述讨论了 Toll 样受体 3(TLR3)缺陷在 HSE 发展中的作用的最新发现。讨论了 TLR3 信号传导中有助于固有反应的关键检查点,包括 TLR3 配体识别位点和细胞内运输的重要性。我们还指出了 TLR3 功能中的未解决问题,这可能导致对 HSE 期间免疫的全面理解。这样的知识库将导致针对 HSE 的合理治疗和预防方法的发现和设计。

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