Models of multiple sclerosis: new insights into pathophysiology and repair

被引:48
作者
Lassmann, Hans [1 ]
机构
[1] Med Univ Vienna, Ctr Brain Res, A-1090 Vienna, Austria
关键词
autoimmune encephalomyelitis; demyelination; multiple sclerosis; neurodegeneration; neuroprotection;
D O I
10.1097/WCO.0b013e3282fee94a
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Purpose of review Experimental models are indispensable in multiple sclerosis research aimed to elucidate the pathogenesis of the disease or to test new therapeutic approaches. The purpose of this review is to discuss the relevance of different models for multiple sclerosis and new insights into pathophysiology of the disease obtained from experimental studies. Recent findings These studies show that tissue damage in the course of brain inflammation is induced by a variety of different components of the immune system, including T cells, autoantibodies and activated effector cells, such as macrophages and microglia. In general, different mechanisms of tissue injury act in parallel and are partly counteracted by the induction of neuroprotective factors and spontaneous regenerative processes. Summary Despite this complexity, experimental studies identified bottlenecks in the destructive process, which can be targeted by therapeutic strategies. To what extent these results can be transferred into therapy of multiple sclerosis has to be shown in the future.
引用
收藏
页码:242 / 247
页数:6
相关论文
共 54 条
[1]   The fibrin-derived γ377-395 peptide inhibits microglia activation and suppresses relapsing paralysis in central nervous system autoimmune disease [J].
Adams, Ryan A. ;
Bauer, Jan ;
Flick, Matthew J. ;
Sikorski, Shoana L. ;
Nuriel, Tal ;
Lassmann, Hans ;
Degen, Jay L. ;
Akassoglou, Katerina .
JOURNAL OF EXPERIMENTAL MEDICINE, 2007, 204 (03) :571-582
[2]   Clonal expansions of CD8+ T cells dominate the T cell infiltrate in active multiple sclerosis lesions as shown by micromanipulation and single cell polymerase chain reaction [J].
Babbe, H ;
Roers, A ;
Waisman, A ;
Lassmann, H ;
Goebels, N ;
Hohlfeld, R ;
Friese, M ;
Schröder, R ;
Deckert, M ;
Schmidt, S ;
Ravid, R ;
Rajewsky, K .
JOURNAL OF EXPERIMENTAL MEDICINE, 2000, 192 (03) :393-404
[3]   Expression of alpha B-crystallin in glia cells during lesional development in multiple sclerosis [J].
Bajramovic, JJ ;
Lassmann, H ;
vanNoort, JM .
JOURNAL OF NEUROIMMUNOLOGY, 1997, 78 (1-2) :143-151
[4]   Axonal protection achieved in a model of multiple sclerosis using lamotrigine [J].
Bechtold, David A. ;
Miller, Sandra J. ;
Dawson, Angela C. ;
Sun, Yue ;
Kapoor, Raju ;
Berry, David ;
Smith, Kenneth J. .
JOURNAL OF NEUROLOGY, 2006, 253 (12) :1542-1551
[5]   Myelin oligodendrocyte glycoprotein-specific T cell receptor transgenic mice develop spontaneous autoimmune optic neuritis [J].
Bettelli, E ;
Pagany, M ;
Weiner, HL ;
Linington, C ;
Sobel, RA ;
Kuchroo, AK .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 197 (09) :1073-1081
[6]   Myelin oligodendrocyte glycoprote in-specific T and B cells cooperate to induce a Devic-like disease in mice [J].
Bettelli, Estelle ;
Baeten, Dominique ;
Jager, Anneli ;
Sobel, Raymond A. ;
Kuchroo, Vijay K. .
JOURNAL OF CLINICAL INVESTIGATION, 2006, 116 (09) :2393-2402
[7]  
BLACK JA, 2006, BRAIN, V129, P3147
[8]   Exacerbation of experimental autoimmune encephalomyelitis after withdrawal of phenytoin and carbamazepine [J].
Black, Joel A. ;
Liu, Shujun ;
Carrithers, Michael ;
Carrithers, Lisette M. ;
Waxman, Stephen G. .
ANNALS OF NEUROLOGY, 2007, 62 (01) :21-33
[9]   Effective and selective immune surveillance of the brain by MHC class I-restricted cytotoxic T lymphocytes [J].
Cabarrocas, J ;
Bauer, J ;
Piaggio, E ;
Liblau, R ;
Lassmann, H .
EUROPEAN JOURNAL OF IMMUNOLOGY, 2003, 33 (05) :1174-1182
[10]   The influence of the proinflammatory cytokine, osteopontin, on autoimmune demyelinating disease [J].
Chabas, D ;
Baranzini, SE ;
Mitchell, D ;
Bernard, CCA ;
Rittling, SR ;
Denhardt, DT ;
Sobel, RA ;
Lock, C ;
Karpuj, M ;
Pedotti, R ;
Heller, R ;
Oksenberg, JR ;
Steinman, L .
SCIENCE, 2001, 294 (5547) :1731-1735