[The role of apoptosis in autoimmune encephalomyelitis].
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.
Okuda
Yoshinobu
Y
Department of Neurology, D-4, Osaka University Graduate School of Medicine.
Sakoda
Saburo
S
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001402:B-Lymphocytes / Q000473:pathology / Q000502:physiology; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000209:etiology* / Q000473:pathology; D006801:Humans; D007962:Leukocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology / Q000502:physiology; D009474:Neurons / Q000473:pathology / Q000502:physiology; D009836:Oligodendroglia / Q000473:pathology / Q000502:physiology; D013601:T-Lymphocytes / Q000473:pathology / Q000502:physiology