Scolding N, Linington C, Compston A
Department of Medicine, University of Wales College of Medicine, Cardiff.
Autoimmunity. 1989;4(1-2):131-42. doi: 10.3109/08916938909034368.
The loss of myelin which characterises many human and experimental demyelinating diseases, among them multiple sclerosis, is thought to be immune mediated, but the precise mechanisms responsible remain unknown despite intense research. Normally, myelin in the central nervous system (CNS) is protected from systemic immune responses by the blood brain barrier, which separates nervous tissue from the peripheral circulation. Here we review evidence suggesting that an understanding of the demyelinating disorders may be helped by considering their immune pathogenesis in two stages. The first is damage to the blood brain barrier; this appears to be cell mediated, and allows infiltration into the CNS of other immune effectors. These include complement and also macrophages, which together may mediate the second stage, injury to the myelin/oligodendrocyte complex.
许多人类和实验性脱髓鞘疾病（包括多发性硬化症）的特征是髓鞘丢失，这种情况被认为是由免疫介导的，但尽管进行了深入研究，其确切机制仍不清楚。正常情况下，中枢神经系统（CNS）中的髓鞘受到血脑屏障的保护，免受全身免疫反应的影响，血脑屏障将神经组织与外周循环分隔开来。在这里，我们回顾相关证据，这些证据表明，分两个阶段考虑脱髓鞘疾病的免疫发病机制，可能有助于理解这些疾病。第一阶段是血脑屏障受损；这似乎是由细胞介导的，并允许其他免疫效应细胞浸润到中枢神经系统。这些效应细胞包括补体以及巨噬细胞，它们共同可能介导第二阶段，即髓鞘/少突胶质细胞复合体的损伤。
