TOLERANCE AND SUPPRESSOR MECHANISMS IN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS - IMPLICATIONS FOR IMMUNOTHERAPY OF HUMAN AUTOIMMUNE-DISEASES

被引：42

作者：

MILLER, A ^{[1
]}

HAFLER, DA ^{[1
]}

WEINER, HL ^{[1
]}

机构：

[1] HARVARD UNIV,SCH MED,BOSTON,MA 02115

来源：

FASEB JOURNAL | 1991年 / 5卷 / 11期

关键词：

AUTOIMMUNITY; IMMUNOTHERAPY; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; TOLERANCE;

D O I：

10.1096/fasebj.5.11.1868980

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：

Recent advances in understanding antigen recognition at the level of the trimolecular complex have provided new approaches for selective immunotherapy. Many of these approaches have been applied successfully to the animal model experimental autoimmune encephalomyelitis, and some are being tested in the human disease multiple sclerosis. In addition, new approaches utilizing nonspecific modulation of immune function are being explored in animals and humans. Immunospecific therapy in autoimmune diseases will ultimately be based on understanding how the normal immune system maintains unresponsiveness to self and how this state of self-tolerance is broken. Strategies for specific immune intervention in human diseases based on components of the trimolecular complex will have to take into account the polymorphism of the major histocompatibility complex in humans and the degree of heterogeneity among autoimmune T cells that react with an autoantigen.

引用

页码：2560 / 2566

页数：7

共 94 条

[51] EVIDENCE FOR FUNCTION OF IA MOLECULES ON GUT EPITHELIAL-CELLS IN MAN [J].