Okuda Yoshinobu, Sakoda Saburo
Department of Neurology, D-4, Osaka University Graduate School of Medicine.
Nihon Rinsho. 2003 Aug;61(8):1323-8.
Experimental autoimmune encephalomyelitis(EAE), an inflammatory demyelinating disease of the central nervous system(CNS) provoked by myelin antigens, is widely used as a model for multiple sclerosis. Recent studies have shown that apoptosis may contribute to the death of oligodendrocytes and/or neurons, a pathological event leading to neurological deficits. On the other hand, the apoptotic elimination of inflammatory cells such as T cells and macrophages from the CNS is generally believed to contribute to the spontaneous recovery of EAE. Thus, apoptosis is involved in the disease-regulating as well as the disease-promoting processes of EAE.
实验性自身免疫性脑脊髓炎（EAE）是一种由髓鞘抗原引发的中枢神经系统（CNS）炎性脱髓鞘疾病，被广泛用作多发性硬化症的模型。最近的研究表明，细胞凋亡可能导致少突胶质细胞和/或神经元死亡，这是一种导致神经功能缺损的病理事件。另一方面，一般认为从CNS中凋亡清除炎性细胞（如T细胞和巨噬细胞）有助于EAE的自发恢复。因此，细胞凋亡参与了EAE的疾病调节以及疾病促进过程。
