Apoptosis in multiple sclerosis.
Several recent studies have provided evidence that apoptosis is an important feature in the pathogenesis of multiple sclerosis (MS), an autoimmune disease of the central nervous system. Apoptosis presumably plays a role in the immunoregulation via activation-induced T-cell death (AICD) and in local processes of tissue damage. In this review the dual role of apoptosis in the MS pathogenesis and its relevance regarding therapeutic concepts is discussed.
Zipp
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Department of Neurology, University Hospital Charité, Berlin, Germany. frauke.zipp@charite.de
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D051017:Apoptosis Regulatory Proteins; D015551:Autoimmunity; D053222:Fas Ligand Protein; D006801:Humans; D008562:Membrane Glycoproteins / Q000502:physiology; D051379:Mice; D008954:Models, Biological; D009103:Multiple Sclerosis / Q000276:immunology* / Q000503:physiopathology* / Q000628:therapy; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000276:immunology / Q000502:physiology; D053221:TNF-Related Apoptosis-Inducing Ligand; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D051017:Apoptosis Regulatory Proteins; C505661:FASLG protein, human; D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D008562:Membrane Glycoproteins; D053221:TNF-Related Apoptosis-Inducing Ligand; C505653:TNFSF10 protein, human; C505654:Tnfsf10 protein, mouse; D014409:Tumor Necrosis Factor-alpha