Sabelko-Downes K A, Russell J H, Cross A H
Department of Molecular Biology, Washington University School of Medicine, St. Louis, MO 63110, USA.
J Neuroimmunol. 1999 Dec;100(1-2):42-52. doi: 10.1016/s0165-5728(99)00191-5.
Multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) represent complex processes that lead to destruction of oligodendrocytes (ODCs) and myelin. T cells are integral to the development of these diseases, but whether T cell-mediated cytolytic mechanisms are involved in the destruction of MHC Class II-negative targets, such as oligodendroglia and myelin, in the CNS is unclear. The primary lytic mechanism employed by CD4+ T cells is Fas-dependent, but can be MHC-unrestricted. Thus, T cell-mediated Fas-FasL interactions could directly contribute to the pathology of EAE and MS. This review summarizes studies from our laboratory and others that implicate Fas-FasL interactions in both the pathogenesis and regulation of demyelinating diseases.
多发性硬化症（MS）和实验性自身免疫性脑脊髓炎（EAE）是导致少突胶质细胞（ODC）和髓鞘破坏的复杂过程。T细胞在这些疾病的发展中不可或缺，但T细胞介导的溶细胞机制是否参与中枢神经系统中MHC II类阴性靶标（如少突胶质细胞和髓鞘）的破坏尚不清楚。CD4 + T细胞采用的主要裂解机制是Fas依赖性的，但可以不受MHC限制。因此，T细胞介导的Fas-FasL相互作用可能直接导致EAE和MS的病理变化。这篇综述总结了我们实验室和其他实验室的研究，这些研究表明Fas-FasL相互作用在脱髓鞘疾病的发病机制和调节中都有涉及。
