The origin and application of experimental autoimmune encephalomyelitis

被引:336
作者
Baxter, Alan G. [1 ]
机构
[1] James Cook Univ N Queensland, Comparat Genom Ctr, Townsville, Qld 4811, Australia
基金
英国医学研究理事会;
关键词
D O I
10.1038/nri2190
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Experimental autoimmune encephalomyelitis (EAE) is a model of the neuroimmune system responding to priming with central nervous system (CNS)-restricted antigens. it is an excellent model of post-vaccinal encephalitis and a useful model of many aspects of multiple sclerosis. EAE has been established in numerous species and is induced by priming with a large number of CNS-derived antigens. As a consequence, the pathogenesis, pathology and clinical signs vary significantly between experimental protocols. As I describe in this Timeline article, the reductionist approach taken in some lines of investigation of EAE resulted in a reliance on results obtained under a narrow range of conditions. Although such studies made important contributions to our molecular understanding of inflammation, T-cell activation, and MHC restriction, they did not advance as effectively our knowledge of the polyantigenic responses that usually occur in CNS immunopathology and autoimmunity.
引用
收藏
页码:904 / 912
页数:10
相关论文
共 101 条
[1]   LIMITED HETEROGENEITY OF T-CELL RECEPTORS FROM LYMPHOCYTES MEDIATING AUTOIMMUNE ENCEPHALOMYELITIS ALLOWS SPECIFIC IMMUNE INTERVENTION [J].
ACHAORBEA, H ;
MITCHELL, DJ ;
TIMMERMANN, L ;
WRAITH, DC ;
TAUSCH, GS ;
WALDOR, MK ;
ZAMVIL, SS ;
MCDEVITT, HO ;
STEINMAN, L .
CELL, 1988, 54 (02) :263-273
[2]   THE MORBID ANATOMY OF THE DEMYELINATIVE DISEASES [J].
ADAMS, RD ;
KUBIK, CS .
AMERICAN JOURNAL OF MEDICINE, 1952, 12 (05) :510-546
[3]  
AMOR S, 1994, J IMMUNOL, V153, P4349
[4]  
Balaguer DDG, 1888, GACETA MED CATALANA, V11, P45
[5]   Human rabies and rabies vaccine encephalomyelitis - A clinicopathologic study [J].
Bassoe, P ;
Grinker, RR .
ARCHIVES OF NEUROLOGY AND PSYCHIATRY, 1930, 23 (06) :1138-1160
[6]   MURINE T-CELL RECEPTOR MUTANTS WITH DELETIONS OF BETA-CHAIN VARIABLE REGION GENES [J].
BEHLKE, MA ;
CHOU, HS ;
HUPPI, K ;
LOH, DY .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1986, 83 (03) :767-771
[7]   THE RAPID ISOLATION OF CLONABLE ANTIGEN-SPECIFIC LYMPHOCYTE-T LINES CAPABLE OF MEDIATING AUTOIMMUNE ENCEPHALOMYELITIS [J].
BENNUN, A ;
WEKERLE, H ;
COHEN, IR .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1981, 11 (03) :195-199
[8]   Encephalitogenic potential of the myelin basic protein peptide (amino acids 83-99) in multiple sclerosis: Results of a phase II clinical trial with an altered peptide ligand [J].
Bielekova, B ;
Goodwin, B ;
Richert, N ;
Cortese, I ;
Kondo, T ;
Afshar, G ;
Gran, B ;
Eaton, J ;
Antel, J ;
Frank, JA ;
McFarland, HF ;
Martin, R .
NATURE MEDICINE, 2000, 6 (10) :1167-1175
[9]   A PILOT TRIAL OF COP-1 IN EXACERBATING REMITTING MULTIPLE-SCLEROSIS [J].
BORNSTEIN, MB ;
MILLER, A ;
SLAGLE, S ;
WEITZMAN, M ;
CRYSTAL, H ;
DREXLER, E ;
KEILSON, M ;
MERRIAM, A ;
WASSERTHEILSMOLLER, S ;
SPADA, V ;
WEISS, W ;
ARNON, R ;
JACOBSOHN, I ;
TEITELBAUM, D ;
SELA, M .
NEW ENGLAND JOURNAL OF MEDICINE, 1987, 317 (07) :408-414
[10]   BOTH RAT AND MOUSE T-CELL RECEPTORS SPECIFIC FOR THE ENCEPHALITOGENIC DETERMINANT OF MYELIN BASIC-PROTEIN USE SIMILAR V-ALPHA AND V-BETA CHAIN GENES EVEN THOUGH THE MAJOR HISTOCOMPATIBILITY COMPLEX AND ENCEPHALITOGENIC DETERMINANTS BEING RECOGNIZED ARE DIFFERENT [J].
BURNS, FR ;
LI, XO ;
SHEN, N ;
OFFNER, H ;
CHOU, YK ;
VANDENBARK, AA ;
HEBERKATZ, E .
JOURNAL OF EXPERIMENTAL MEDICINE, 1989, 169 (01) :27-39