Antigen-specific tolerance strategies for the prevention and treatment of autoimmune disease

被引：238

作者：

Miller, Stephen D. ^{[1
]}

Turley, Danielle M. ^{[1
]}

Podojil, Joseph R. ^{[1
]}

机构：

[1] Northwestern Univ, Immunobiol Ctr, Dept Microbiol Immunol & Interdepartmental, Feinberg Sch Med, Chicago, IL 60611 USA

来源：

NATURE REVIEWS IMMUNOLOGY | 2007年 / 7卷 / 09期

关键词：

D O I：

10.1038/nri2153

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The development of safe and effective antigen-specific therapies is needed to treat patients with autoimmune diseases. These therapies must allow for the specific tolerization of self-reactive immune cells without altering host immunity to infectious insults. Experimental models and clinical trials for the treatment of autoimmune disease have identified putative mechanisms by which antigen-specific therapies induce tolerance. Although advances have been made in the development of efficient antigen-specific therapies, translating these therapies from bench to bedside has remained difficult. Here, we discuss the recent advances in our understanding of antigen-specific therapies for the treatment of autoimmune diseases.

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页码：665 / 677

页数：13

相关论文

共 122 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] Immunomodulation in type 1 diabetes by NBI-6024, an altered peptide ligand of the insulin B(9-23) epitope [J].

Alleva, DG ;

Maki, RA ;

Putnam, AL ;

Robinson, JM ;

Kipnes, MS ;

Dandona, P ;

Marks, JB ;

Simmons, DL ;

Greenbaum, CJ ;

Jimenez, RG ;

Conlon, PJ ;

Gottlieb, PA .

SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 2006, 63 (01) :59-69

[3] GRAIL:: An E3 ubiquitin ligase that inhibits cytokine gene transcription is expressed in anergic CD4+ T cells [J].

Anandasabapathy, N ;

Ford, GS ;

Bloom, D ;

Holness, C ;

Paragas, V ;

Seroogy, C ;

Skrenta, H ;

Hollenhorst, M ;

Fathman, CG ;

Soares, L .

IMMUNITY, 2003, 18 (04) :535-547

[4] 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

[5]

Bai XF, 1998, CLIN EXP IMMUNOL, V111, P205

[6] CNS myeloid DCs presenting endogenous myelin peptides 'preferentially' polarize CD4+ TH-17 cells in relapsing EAE [J].

Bailey, Samantha L. ;

Schreiner, Bettina ;

McMahon, Eileen J. ;

Miller, Stephen D. .

NATURE IMMUNOLOGY, 2007, 8 (02) :172-180

[7]

Barnett ML, 1998, ARTHRITIS RHEUM, V41, P290, DOI 10.1002/1529-0131(199802)41:2<290::AID-ART13>3.3.CO

[8]

2-I

[9] TGF-β-dependent mechanisms mediate restoration of self-tolerance induced by antibodies to CD3 in overt autoimmune diabetes [J].

Belghith, M ;

Bluestone, JA ;

Barriot, S ;

Mégret, J ;

Bach, JF ;

Chatenoud, L .

NATURE MEDICINE, 2003, 9 (09) :1202-1208

[10]

Benson JM, 1999, J IMMUNOL, V162, P6247

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