Boccaccio G L, Steinman L
Department of Immunology, Weizmann Institute of Science, Rehovot, Israel.
J Neurosci Res. 1996 Sep 15;45(6):647-54. doi: 10.1002/(SICI)1097-4547(19960915)45:6<647::AID-JNR1>3.0.CO;2-8.
Multiple sclerosis (MS) is a demyelinating disease during which an autoimmune reaction is directed against oligodendrocytes. Alterations of normal myelin structure or oligodendrocyte metabolism may be primary events that influence the susceptibility to MS. Once triggered, the immune system attacks and destroys myelin and the myelin forming cell. Evidence is presented that the oligodendrocyte responds to the attack by immune cells and their secreted products through modulation of its metabolism and gene expression. Cytokines, immunoglobulins, and complement complexes may elicit a survival response in the oligodendrocytes, involving the induction of heat shock proteins and other protective molecules. The possibility of manipulating these complex glial cell functions and controlling their pathologic interactions with immune cells will illuminate how myelin damage can be contained and how the injured tissue can be repaired.
多发性硬化症（MS）是一种脱髓鞘疾病，在此期间，自身免疫反应针对少突胶质细胞。正常髓鞘结构或少突胶质细胞代谢的改变可能是影响MS易感性的主要事件。一旦触发，免疫系统就会攻击并破坏髓鞘和形成髓鞘的细胞。有证据表明，少突胶质细胞通过调节其代谢和基因表达来响应免疫细胞及其分泌产物的攻击。细胞因子、免疫球蛋白和补体复合物可能在少突胶质细胞中引发存活反应，包括诱导热休克蛋白和其他保护分子。操纵这些复杂的神经胶质细胞功能并控制它们与免疫细胞的病理相互作用的可能性，将阐明如何抑制髓鞘损伤以及如何修复受损组织。
