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髓鞘相关糖蛋白、髓磷脂碱性蛋白和P0蛋白在泰勒氏病毒感染的急性和复发性脱髓鞘病变中的免疫细胞化学定位

Immunocytochemical localization of MAG, MBP and P0 protein in acute and relapsing demyelinating lesions of Theiler's virus infection.

作者信息

Dal Canto M C, Barbano R L

出版信息

J Neuroimmunol. 1985 Dec;10(2):129-40. doi: 10.1016/0165-5728(85)90003-7.

Abstract

Acute demyelinating and relapsing demyelinating lesions from spinal cords of mice infected with the WW strain of Theiler's encephalomyelitis virus (TMEV) were studied immunocytochemically with antisera to various myelin constituents. Acute lesions were studied for differences in the distribution of myelin basic protein (MBP) and myelin associated glycoprotein (MAG). Relapsing lesions, characterized by demyelination of areas previously remyelinated by Schwann cells, were studied for differences in the distribution of P0 and MAG. In both instances the earliest lesions were characterized by preferential disappearance of MBP and P0 respectively when compared to MAG. In well-developed lesions, MAG, MBP and P0 were absent in essentially equal proportion. These observations are in agreement with previous findings suggesting a primary loss of myelin rather than a direct attack on oligodendrocytes as the main pathogenetic mechanism of demyelination in this viral model.

摘要

用针对各种髓磷脂成分的抗血清,对感染泰勒氏脑脊髓炎病毒(TMEV)WW株的小鼠脊髓中的急性脱髓鞘和复发性脱髓鞘病变进行了免疫细胞化学研究。研究急性病变中髓磷脂碱性蛋白(MBP)和髓磷脂相关糖蛋白(MAG)分布的差异。复发性病变的特征是先前由施万细胞重新髓鞘化的区域发生脱髓鞘,研究P0和MAG分布的差异。在这两种情况下,与MAG相比,最早的病变分别以MBP和P0的优先消失为特征。在发育良好的病变中,MAG、MBP和P0基本以相等的比例缺失。这些观察结果与先前的发现一致,表明髓磷脂的原发性丧失而非对少突胶质细胞的直接攻击是该病毒模型中脱髓鞘的主要发病机制。

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