Apoptosis in multiple sclerosis - Etiopathogenetic relevance and perspectives for new therapeutic strategies [Apoptose bei multipler sklerose. Atiopathogenetische relevanz und perspektiven fur neue therapeutische strategien]

被引：0
作者：
Aktas O. [1 ]
Wendling U. [1 ]
Zschenderlein R. [1 ]
Zipp F. [1 ]
机构：
[1] Neurologische Klinik und Poliklinik, Medizinische Fakultät der Humboldt, Universität Berlin
来源：
Der Nervenarzt | 2000年 / 71卷 / 10期
关键词：
Apoptosis; CD95; Immunopathogenesis; Multiple sclerosis; TNF;
D O I：
10.1007/s001150050664
中图分类号：
学科分类号：
摘要：
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.
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页码：767 / 773
页数：6
相关论文
共 38 条
[1]  
Bachmann R., Eugster H.P., Frei K., Fontana A., Lassmann H., Impairmen: Of TNF-receptor-1 signaling but not Fas signaling diminishes T-cell apoptosis in myelin oligodendrocyte glycoprotein peptide-induced chronic demyelinating autoimmune encephalomyelitis in mice, Am J Pathol, 154, pp. 1417-1422, (1999)
[2]  
Bechmann I., Mor G., Nilsen J., Eliza M., Nitsch R., Naftolin F., FasL (CD95L,Apo1L) is expressed in the normal rat and human brain: Evidence for the existence of an immunological brain barrier, Glia, 27, pp. 62-74, (1999)
[3]  
Bonetti B., Raine C.S., Multiple sclerosis: Oligodendrocytes display cell death-related molecules in situ but do not undergo apoptosis, Ann Neurol, 42, pp. 74-84, (1997)
[4]  
Carrieri P.B., Provitera V., Bruno R., Perella M., Tartaglia G., Busto A., Perrella O., Possible role of transforming growth factor-beta in relapsing-remitting multiple sclerosis, Neurol Res, 19, pp. 599-600, (1997)
[5]  
Cheng J., Zhou T., Liu C., Et al., Protection from Fas-mediated apoptosis by a soluble form of the Fas molecule, Science, 263, pp. 1759-1762, (1994)
[6]  
Clark R.B., Grunnet M., Lingenheld E.G., Adoptively transferred EAE in mice bearing the Ipr mutation, Clin Immunol Immunpathol, 8 S, pp. 315-319, (1997)
[7]  
Critchfield J.M., Racke M.K., Zuniga-Pflucker J.C., Cannella B., Raine C.S., Goverman J., Lenardo M.J., T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis, Science, 263, pp. 1139-1143, (1994)
[8]  
D'Souza S.D., Bonetti B., Balasingam V., Cashman N.R., Barker P.A., Troutt A.B., Raine C.S., Antel J.P., Multiple sclerosis: Fas signaling in oligodendrocyte cell death, J Exp Med, 184, pp. 2361-2370, (1996)
[9]  
Dittel B.N., Merchant R.M., Janeway C.A., Evidence for Fas-dependent and Fas-independent mechanisms in the pathogenesis of experimental autoimmune encephalomyelitis, J Immunol, 162, pp. 6392-6400, (1999)
[10]  
Dowling P., Husar W., Menonna J., Cook S., Sidhu M., Cell death and birth in multiple sclerosis brain, J Neurol Sci, 149, pp. 1-11, (1997)
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