IMMUNOTHERAPEUTIC STRATEGIES DIRECTED AT THE TRIMOLECULAR COMPLEX

被引:21
作者
GAUR, A
FATHMAN, CG
机构
[1] Department of Medicine, Division of Immunology and Rheumatology, Stanford University Medical Center
来源
ADVANCES IN IMMUNOLOGY, VOLUME 56 | 1994年 / 56卷
关键词
D O I
10.1016/S0065-2776(08)60453-8
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
This chapter discusses earlier experience in preventing the formation of the ternary complex and discusses some newer attempts to induce unresponsiveness in experimental animals. The three components of the complex serve as independent targets for development of strategies aimed at disrupting the trimolecular complex. The earliest attempts at immunotherapy targeting the T cell used anti-lymphocyte serum and monoclonal antibodies directed at the Thy-1 antigen, a marker for all T cells, to eliminate or downregulate T cell activation. The development of hybridoma technology made available reagents, which could target a specific cell population. The chapter discusses the use of antibodies directed at various proteins on the T cell surface in regulating T cell responses, examines T cells as effectors of immune regulation. This approach involves the use of antigen-specific T cell lines or clones as vaccinating agents to elicit “anti-idiotypic” regulator T cells capable of inhibiting the response of the antigen-specific T cell population. As opposed to passive administration of antibodies, this approach involves active participation of the individual's immune system in inducing a regulatory response to the immunizing cells. Among the potential immunotherapeutic strategies outlined in this chapter the most favored is the therapy that is most selective in turning off autoantigen-specific T cells while sparing the rest of the immune response. © 1994, Academic Press Inc.
引用
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页码:219 / 265
页数:47
相关论文
共 241 条
[1]   T-CELL RECEPTORS IN MURINE AUTOIMMUNE-DISEASES [J].
ACHAORBEA, H ;
STEINMAN, L ;
MCDEVITT, HO .
ANNUAL REVIEW OF IMMUNOLOGY, 1989, 7 :371-405
[2]   THE 1ST EXTERNAL DOMAIN OF THE NONOBESE DIABETIC MOUSE CLASS-II I-A BETA-CHAIN IS UNIQUE [J].
ACHAORBEA, H ;
MCDEVITT, HO .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1987, 84 (08) :2435-2439
[3]   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
[4]  
ADORINI L, 1989, IMMUNE RESPONSE TO STRUCTURALLY DEFINED PROTEINS : THE LYSOZYME MODEL, P257
[5]   EXOGENOUS PEPTIDES COMPETE FOR THE PRESENTATION OF ENDOGENOUS ANTIGENS TO MAJOR HISTOCOMPATIBILITY COMPLEX CLASS II-RESTRICTED T-CELLS [J].
ADORINI, L ;
MORENO, J ;
MOMBURG, F ;
HAMMERLING, GJ ;
GUERY, JC ;
VALLI, A ;
FUCHS, S .
JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 174 (04) :945-948
[6]   INVIVO COMPETITION BETWEEN SELF PEPTIDES AND FOREIGN ANTIGENS IN T-CELL ACTIVATION [J].
ADORINI, L ;
MULLER, S ;
CARDINAUX, F ;
LEHMANN, PV ;
FALCIONI, F ;
NAGY, ZA .
NATURE, 1988, 334 (6183) :623-625
[7]   IMMUNOMODULATION OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS BY ANTIBODIES TO THE ANTIGEN-IA COMPLEX [J].
AHARONI, R ;
TEITELBAUM, D ;
ARNON, R ;
PURI, J .
NATURE, 1991, 351 (6322) :147-150
[8]   HYPOTHERMIA AND HYPOGLYCEMIA INDUCED BY ANTI-CD3 MONOCLONAL-ANTIBODY IN MICE - ROLE OF TUMOR-NECROSIS-FACTOR [J].
ALEGRE, M ;
VANDENABEELE, P ;
FLAMAND, V ;
MOSER, M ;
LEO, O ;
ABRAMOWICZ, D ;
URBAIN, J ;
FIERS, W ;
GOLDMAN, M .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1990, 20 (03) :707-710
[9]   ANTI-CD4 MEDIATES CLONAL ANERGY DURING TRANSPLANTATION TOLERANCE INDUCTION [J].
ALTERS, SE ;
SHIZURU, JA ;
ACKERMAN, J ;
GROSSMAN, D ;
SEYDEL, KB ;
FATHMAN, CG .
JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 173 (02) :491-494
[10]  
ALTERS SE, 1989, J IMMUNOL, V142, P2018