Brosnan C F, Raine C S
Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Brain Pathol. 1996 Jul;6(3):243-57. doi: 10.1111/j.1750-3639.1996.tb00853.x.
In this review, we address current concepts regarding the mechanisms of tissue damage that lead to demyelination and oligodendrocyte loss in multiple sclerosis. Particular emphasis has been placed on examining the MS lesion for evidence for pathogenetic processes that have been implicated from various in vivo and in vitro model systems. Central in this analysis has been the evaluation of the various effector cell types and their products. The results strongly support the conclusion that proinflammatory cytokines are major mediators of tissue damage, through the activation of inflammatory cells and resident glial cells. A role for antibody is also discussed, particularly as part of an antibody-dependent cell mediated demyelinating process. Minor populations of lymphocytes may also participate by defining the nature of the immunological microenvironment.
在本综述中,我们阐述了当前关于导致多发性硬化症脱髓鞘和少突胶质细胞丢失的组织损伤机制的概念。特别着重于检查多发性硬化症病变,以寻找来自各种体内和体外模型系统中涉及的致病过程的证据。该分析的核心是评估各种效应细胞类型及其产物。结果有力地支持了以下结论:促炎细胞因子通过激活炎症细胞和驻留神经胶质细胞,是组织损伤的主要介质。还讨论了抗体的作用,特别是作为抗体依赖性细胞介导的脱髓鞘过程的一部分。少数淋巴细胞群体也可能通过确定免疫微环境的性质而参与其中。