Lassmann H
Institute of Neurology, University of Vienna, Austria.
Mult Scler. 1998 Jun;4(3):93-8. doi: 10.1177/135245859800400301.
Multiple sclerosis lesions are characterized by inflammation, demyelination and a variable degree of axonal loss. The patterns of inflammation in MS lesions are compatible with a T-lymphocyte mediated immune reaction. The formation of demyelinated plaques, however, seem to require additional immunological mechanisms. In this review evidence is discussed for a pathogenetic role of demyelinating antibodies, toxic macrophage products, cytotoxic T-cells as well as metabolic disturbances of oligodendrocytes. It is suggested that the pathological heterogeneity regarding the patterns and extent of demyelination, remyelination and axonal loss may be the outcome of variable dominant immunopathogenetic mechanisms in different multiple sclerosis patients.
多发性硬化症病变的特征是炎症、脱髓鞘以及不同程度的轴突损失。多发性硬化症病变中的炎症模式与T淋巴细胞介导的免疫反应相符。然而，脱髓鞘斑块的形成似乎需要额外的免疫机制。在这篇综述中，我们讨论了脱髓鞘抗体、毒性巨噬细胞产物、细胞毒性T细胞以及少突胶质细胞代谢紊乱在发病机制中的作用证据。有人提出，脱髓鞘、再髓鞘化和轴突损失的模式和程度方面的病理异质性可能是不同多发性硬化症患者中不同主导免疫发病机制的结果。
