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周围神经损伤会导致中枢神经系统中主要组织相容性复合体抗原水平升高。

Peripheral nerve lesion produces increased levels of major histocompatibility complex antigens in the central nervous system.

作者信息

Streit W J, Graeber M B, Kreutzberg G W

机构信息

Department of Neuromorphology, Max Planck Institute of Psychiatry, Martinsried, F.R.G.

出版信息

J Neuroimmunol. 1989 Feb;21(2-3):117-23. doi: 10.1016/0165-5728(89)90167-7.

DOI:10.1016/0165-5728(89)90167-7
PMID:2913044
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7119897/
Abstract

Proliferation of central nervous system (CNS) glia in response to peripheral nerve injury occurs without apparent participation of cells of the immune system. It is shown here that following transection of the rat facial nerve there is strongly elevated expression of class I, and to a lesser extent, class II antigens of the major histocompatibility complex (MHC) in the facial nucleus. It is demonstrated by double-immunofluorescence studies that the cells responsible for increased levels of MHC class I antigens are endogenous brain microglia. These findings emphasize the thought that microglia are immunocompetent cells, but, at the same time, raise the possibility for a non-immunological function of MHC antigens under conditions of neural regeneration.

摘要

中枢神经系统(CNS)胶质细胞对周围神经损伤的增殖反应在没有免疫系统细胞明显参与的情况下发生。本文表明,大鼠面神经横断后,面神经核中主要组织相容性复合体(MHC)的I类抗原表达强烈升高,II类抗原表达程度较轻。双重免疫荧光研究表明,负责MHC I类抗原水平升高的细胞是内源性脑小胶质细胞。这些发现强调了小胶质细胞是具有免疫活性的细胞这一观点,但同时也提出了在神经再生条件下MHC抗原具有非免疫功能的可能性。