Mouse models for multiple sclerosis: Historical facts and future implications

被引:132
作者
Croxford, Andrew L. [1 ]
Kurschus, Florian C. [1 ]
Waisman, Ari [1 ]
机构
[1] Johannes Gutenberg Univ Mainz, Univ Med Ctr, Inst Mol Med, D-6500 Mainz, Germany
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2011年 / 1812卷 / 02期
关键词
Multiple sclerosis; Experimental autoimmune encephalomyelitis; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; T-CELL-RECEPTOR; MYELIN OLIGODENDROCYTE GLYCOPROTEIN; CENTRAL-NERVOUS-SYSTEM; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; ANTIGEN-PRESENTING CELLS; TRANSGENIC MICE; INTERFERON-BETA; BASIC-PROTEIN; GLATIRAMER ACETATE;
D O I
10.1016/j.bbadis.2010.06.010
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Multiple sclerosis sclerosis (MS) is an inflammatory and demyelinating condition of the CNS, characterized by perivascular infiltrates composed largely of T lymphocytes and macrophages. Although the precise cause remains unknown, numerous avenues of research support the hypothesis that autoimmune mechanisms play a major role in the development of the disease. Pathologically similar lesions to those seen in MS can be induced in laboratory rodents by immunization with CNS-derived antigens. This form of disease induction, broadly termed experimental autoimmune encephalomyelitis, is frequently the starting point in MS research with respect to studying pathogenesis and creating novel treatments. Many different EAE models are available, each mimicking a particular facet of MS. These models all have common ancestry, and have developed from a single concept of immunization with self-antigen. We will discuss the major changes in immunology research, which have shaped the EAE models we use today, and discuss how current animal models of MS have resulted in successful treatments and more open questions for researchers to address. (C) 2010 Elsevier B.V. All rights reserved.
引用
收藏
页码:177 / 183
页数:7
相关论文
共 98 条
[91]  
Wildbaum G, 1998, J IMMUNOL, V161, P6368
[92]  
Willenborg DO, 1996, J IMMUNOL, V157, P3223
[93]   T-bet is essential for encephalitogenicity of both Th1 and Th17 cells [J].
Yang, Yuhong ;
Weiner, Jeffrey ;
Liu, Yue ;
Smith, Alan J. ;
Huss, David J. ;
Winger, Ryan ;
Peng, Haiyan ;
Cravens, Petra D. ;
Racke, Michael K. ;
Lovett-Racke, Amy E. .
JOURNAL OF EXPERIMENTAL MEDICINE, 2009, 206 (07) :1549-1564
[94]   Interferon β-modulates experimental autoimmune encephalomyelitis by altering the pattern of cytokine secretion [J].
Yasuda, CL ;
Al-Sabbagh, A ;
Oliveira, EC ;
Diaz-Bardales, BM ;
Garcia, AA ;
Santos, LMB .
IMMUNOLOGICAL INVESTIGATIONS, 1999, 28 (2-3) :115-126
[95]   PREVENTION OF EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS BY ANTIBODIES AGAINST ALPHA-4-BETA-1 INTEGRIN [J].
YEDNOCK, TA ;
CANNON, C ;
FRITZ, LC ;
SANCHEZMADRID, F ;
STEINMAN, L ;
KARIN, N .
NATURE, 1992, 356 (6364) :63-66
[96]   Involvement of Th17 cells and the effect of anti-IL-6 therapy in autoimmune uveitis [J].
Yoshimura, Takeru ;
Sonoda, Koh-Hei ;
Ohguro, Nobuyuki ;
Ohsugi, Yoshiyuki ;
Ishibashi, Tatsuro ;
Cua, Daniel J. ;
Kobayashi, Takashi ;
Yoshida, Hiroki ;
Yoshimura, Akihiko .
RHEUMATOLOGY, 2009, 48 (04) :347-354
[97]   Interferon-beta inhibits progression of relapsing-remitting experimental autoimmune encephalomyelitis [J].
Yu, M ;
Nishiyama, A ;
Trapp, BD ;
Tuohy, VK .
JOURNAL OF NEUROIMMUNOLOGY, 1996, 64 (01) :91-100
[98]   Plasticity of CD4+ T Cell Lineage Differentiation [J].
Zhou, Liang ;
Chong, Mark M. W. ;
Littman, Dan R. .
IMMUNITY, 2009, 30 (05) :646-655