Immune modulating peptides for the treatment and suppression of multiple sclerosis

被引:27
作者
Badawi, Ahmed H. [1 ]
Siahaan, Teruna J. [1 ]
机构
[1] Univ Kansas, Dept Pharmaceut Chem, Lawrence, KS 66047 USA
基金
美国国家卫生研究院;
关键词
Multiple sclerosis; Experimental autoimmune encephalomyelitis; Peptide; Antigen; Bifunctional peptide inhibitor; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MYELIN BASIC-PROTEIN; T-CELL-ACTIVATION; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; TUMOR-NECROSIS-FACTOR; 1-PHOSPHATE RECEPTOR MODULATOR; ANTIGEN-SPECIFIC SUPPRESSION; AMINO-ACID COPOLYMERS; TOLL-LIKE RECEPTORS; EPSTEIN-BARR-VIRUS;
D O I
10.1016/j.clim.2012.05.010
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Multiple sclerosis (MS) is a neurodegenerative disease in which the immune system recognizes proteins of the myelin sheath as antigenic, thus initiating an inflammatory reaction in the central nervous system. This leads to demyelination of the axons, breakdown of the blood brain barrier, and lesion formation. Current therapies for the treatment of MS are generally nonspecific and weaken the global immune system, thus making the individual susceptible to opportunistic infections. Antigenic peptides and their derivatives are becoming more prevalent for investigation as therapeutic agents for MS because they possess immune-specific characteristics. In addition, other peptides that target vital components of the inflammatory immune response have also been developed. Therefore, the objectives of this review are to (a) summarize the immunological basis for the development of MS, (b) discuss specific and nonspecific peptides tested in EAE and in humans, and (c) briefly address some problems and potential solutions with these novel therapies. (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码:127 / 138
页数:12
相关论文
共 164 条
[1]
Copolymer 1 acts against the immunodominant epitope 82-100 of myelin basic protein by T cell receptor antagonism in addition to major histocompatibility complex blocking [J].
Aharoni, R ;
Teitelbaum, D ;
Arnon, R ;
Sela, M .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (02) :634-639
[2]
Epitope-specific T cell tolerance to phospholipase A(2) in bee venom immunotherapy and recovery by IL-2 and IL-15 in vitro [J].
Akdis, CA ;
Akdis, M ;
Blesken, T ;
Wymann, D ;
Alkan, SS ;
Muller, U ;
Blaser, K .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 98 (07) :1676-1683
[3]
ANTIGEN-DRIVEN TISSUE-SPECIFIC SUPPRESSION FOLLOWING ORAL TOLERANCE - ORALLY-ADMINISTERED MYELIN BASIC-PROTEIN SUPPRESSES PROTEOLIPID PROTEIN-INDUCED EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS IN THE SJL MOUSE [J].
ALSABBAGH, A ;
MILLER, A ;
SANTOS, LMB ;
WEINER, HL .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1994, 24 (09) :2104-2109
[4]
Anderton SM, 1998, EUR J IMMUNOL, V28, P1251, DOI 10.1002/(SICI)1521-4141(199804)28:04<1251::AID-IMMU1251>3.0.CO
[5]
2-O
[6]
[Anonymous], COCHRANE DATABASE SY, DOI 10.1002/14651858.CD004678
[8]
Modulation of T-cell activation by the glucocorticoid-induced leucine zipper factor via inhibition of nuclear factor κB [J].
Ayroldi, E ;
Migliorati, G ;
Bruscoli, S ;
Marchetti, C ;
Zollo, O ;
Cannarile, L ;
D'Adamio, F ;
Riccardi, C .
BLOOD, 2001, 98 (03) :743-753
[9]
Epstein-barr virus in multiple sclerosis [J].
Bagert, Bridget A. .
CURRENT NEUROLOGY AND NEUROSCIENCE REPORTS, 2009, 9 (05) :405-410
[10]
Nasal administration of myelin basic protein prevents relapsing experimental autoimmune encephalomyelitis in DA rats by activating regulatory cells expressing IL-4 and TGF-beta mRNA [J].
Bai, XF ;
Shi, FD ;
Xiao, BG ;
Li, HL ;
vanderMeide, PH ;
Link, H .
JOURNAL OF NEUROIMMUNOLOGY, 1997, 80 (1-2) :65-75