[Apoptosis in multiple sclerosis. Etiopathogenetic relevance and prospects for new therapeutic strategies].
Apoptosis, or programmed cell death, is a physiological cell suicide program mainly leading to selective elimination of useless cells. This mechanism is important for the homeostasis of the immune system and presumably plays a two-sided role in the pathogenesis of multiple sclerosis (MS). On the one hand, evidence has been provided that impaired apoptosis might result in increased numbers or persistence of activated myelin-specific T cells, thus inducing the pathophysiologic processes in MS. On the other hand, local tissue damage might involve apoptosis of glial and neuronal cells and lead to the clinical symptoms. Here, an overview is presented on the current knowledge of the role of apoptosis in the pathogenesis of MS, and implications for related therapeutic strategies are discussed.
Aktas
O
O
Neurologische Klinik und Poliklinik, Medizinische Fakultät der Humboldt-Universität Berlin.
Wendling
U
U
Zschenderlein
R
R
Zipp
F
F
D017209:Apoptosis / Q000276:immunology*; D001324:Autoantigens / Q000276:immunology*; D006801:Humans; D007165:Immunosuppression Therapy; D008213:Lymphocyte Activation / Q000276:immunology*; D009103:Multiple Sclerosis / Q000276:immunology* / Q000628:therapy; D009185:Myelin Proteins / Q000276:immunology; D009457:Neuroglia / Q000276:immunology; D009474:Neurons / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D001324:Autoantigens; D009185:Myelin Proteins