Potential role of humoral immunity in the pathogenesis of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE)

被引:20
作者
del Pilar Martin, Maria
Monson, Nancy L.
机构
[1] Univ Texas, SW Med Ctr, Dept Neurol, Dallas, TX 75390 USA
[2] Univ Texas, SW Med Ctr, Ctr Immunol, Dallas, TX 75390 USA
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2007年 / 12卷
关键词
B cells; antibody; complement; humoral immunity; multiple sclerosis; experimental autoimmune encephalomyelitis; review;
D O I
10.2741/2268
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
The earliest research literature addressing subclinical characteristics of Multiple Sclerosis was largely focused on humoral immune components, particularly antibodies in the cerebrospinal fluid of MS patients. However, two decades later, in the 1990's, T cells were established as a major component of the underlying mechanism( s) of MS pathogenesis, especially since EAE, the mouse model of MS, could be readily induced by immunization with myelin derived peptides or passive transfer of encephalogenic T cells. This data has contributed to the concept that the role of humoral immunity in MS pathogenesis may be negligible. However, more recent studies have provided important insights regarding the role of humoral immunity in MS pathogenesis. The goals of this review are to 1) summarize evidence for and against the hypothesis that humoral immunity plays a central role in the pathogenesis of MS, and 2) summarize studies in the EAE model that directly tested the role of humoral immunity in pathogenesis of the disease. With this information, we hope to convince the reader that great strides have been made towards defining a central role of humoral immunity in MS pathogenesis, but that there is a substantial amount of work to be done ( especially in the EAE model) to ensure that the contribution of humoral immunity to MS pathogenenesis is effectively addressed.
引用
收藏
页码:2735 / 2749
页数:15
相关论文
共 128 条
[1]  
Alt C, 2002, EUR J IMMUNOL, V32, P2133, DOI 10.1002/1521-4141(200208)32:8<2133::AID-IMMU2133>3.0.CO
[2]  
2-W
[3]   CEREBROSPINAL-FLUID IN THE DIAGNOSIS OF MULTIPLE-SCLEROSIS - A CONSENSUS REPORT [J].
ANDERSSON, M ;
ALVAREZCERMENO, J ;
BERNARDI, G ;
COGATO, I ;
FREDMAN, P ;
FREDERIKSEN, J ;
FREDRIKSON, S ;
GALLO, P ;
GRIMALDI, LM ;
GRONNING, M ;
KEIR, G ;
LAMERS, K ;
LINK, H ;
MAGALHAES, A ;
MASSARO, AR ;
OHMAN, S ;
REIBER, H ;
RONNBACK, L ;
SCHLUEP, M ;
SCHULLER, E ;
SINDIC, CJM ;
THOMPSON, EJ ;
TROJANO, M ;
WURSTER, U .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 1994, 57 (08) :897-902
[4]  
Archelos JJ, 2000, ANN NEUROL, V47, P694, DOI 10.1002/1531-8249(200006)47:6<694::AID-ANA2>3.3.CO
[5]  
2-N
[6]   Pathogenetic role of autoantibodies in neurological diseases [J].
Archelos, JJ ;
Hartung, HP .
TRENDS IN NEUROSCIENCES, 2000, 23 (07) :317-327
[7]  
Baranzini SE, 1999, J IMMUNOL, V163, P5133
[8]   Antimyelin antibodies as a predictor of clinically definite multiple sclerosis after a first demyelinating event [J].
Berger, T ;
Rubner, P ;
Schautzer, F ;
Egg, R ;
Ulmer, H ;
Mayringer, I ;
Dilitz, E ;
Deisenhammer, F ;
Reindl, M .
NEW ENGLAND JOURNAL OF MEDICINE, 2003, 349 (02) :139-145
[9]   Highly related immunoglobulin light chain sequences in different multiple sclerosis patients [J].
Blalock, JE ;
Zhou, SR ;
Maier, CC ;
Galin, FS ;
Whitaker, JN .
JOURNAL OF NEUROIMMUNOLOGY, 1999, 100 (1-2) :98-101
[10]  
BOOS L, 2004, GLIA