Cytokine shifts and tolerance in experimental autoimmune encephalomyelitis

被引:59
作者
Chitnis, T [1 ]
Khoury, SJ [1 ]
机构
[1] Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA
关键词
experimental autoimmune encephalomyelitis; multiple sclerosis; tolerance; cytokines; T-helper cell; T cell; STAT;
D O I
10.1385/IR:28:3:223
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Cytokines play an important role in the pathogenesis of both multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). Effective treatments for both diseases have been shown to alter cytokines in the central nervous system and in activated mononuclear cells. EAE is an animal model that mimics many aspects of multiple sclerosis, and has been widely used to study the mechanisms of disease and therapeutic approaches to multiple sclerosis. Cytokines play an important role in regulation of disease expression in EAE, and in tolerance to disease induction. In this review, we will summarize the current findings on the role of cytokine shifts in the induction of tolerance in EAE. In addition, we will discuss modulation of EAE by altered expression of members of the cytokine-regulated Jak/STAT intracellular signaling pathway.
引用
收藏
页码:223 / 239
页数:17
相关论文
共 126 条
[1]   Oligodendrocyte apoptosis and primary demyelination induced by local TNF/p55TNF receptor signaling in the central nervous system of transgenic mice - Models for multiple sclerosis with primary oligodendrogliopathy [J].
Akassoglou, K ;
Bauer, J ;
Kassiotis, G ;
Pasparakis, M ;
Lassmann, H ;
Kollias, G ;
Probert, L .
AMERICAN JOURNAL OF PATHOLOGY, 1998, 153 (03) :801-813
[2]   Impairment 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 [J].
Bachmann, R ;
Eugster, HP ;
Frei, K ;
Fontana, A ;
Lassmann, H .
AMERICAN JOURNAL OF PATHOLOGY, 1999, 154 (05) :1417-1422
[3]   Regulation of antigen-specific CD8+ T cell homeostasis by perforin and interferon-γ [J].
Badovinac, VP ;
Tvinnereim, AR ;
Harty, JT .
SCIENCE, 2000, 290 (5495) :1354-1357
[4]   Defective regulation of IFNγ and IL-12 by endogenous IL-10 in progressive MS [J].
Balashov, KE ;
Comabella, M ;
Ohashi, T ;
Khoury, SJ ;
Weiner, HL .
NEUROLOGY, 2000, 55 (02) :192-198
[5]   Increased interleukin 12 production in progressive multiple sclerosis: Induction by activated CD4(+) T cells via CD40 ligand [J].
Balashov, KE ;
Smith, DR ;
Khoury, SJ ;
Hafler, DA ;
Weiner, HL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (02) :599-603
[6]  
Barbulescu K, 1998, J IMMUNOL, V160, P3642
[7]  
Begolka WS, 1998, J IMMUNOL, V161, P4437
[8]  
Bettelli E, 1998, J IMMUNOL, V161, P3299
[9]   Expression of IL-12 in CNS and lymphoid organs of mice with experimental allergic encephalitis [J].
Bright, JJ ;
Musuro, BF ;
Du, C ;
Sriram, S .
JOURNAL OF NEUROIMMUNOLOGY, 1998, 82 (01) :22-30
[10]   CYTOKINE LOCALIZATION IN MULTIPLE-SCLEROSIS LESIONS - CORRELATION WITH ADHESION MOLECULE EXPRESSION AND REACTIVE NITROGEN SPECIES [J].
BROSNAN, CF ;
CANNELLA, B ;
BATTISTINI, L ;
RAINE, CS .
NEUROLOGY, 1995, 45 (06) :S16-S21