Normal incidence of diabetes in NOD mice tolerant to glutamic acid decarboxylase

被引：73

作者：

Jaeckel, E

Klein, L

Martin-Orozco, N

von Boehmer, H

机构：

[1] Harvard Univ, Dana Farber Canc Inst, Sch Med, Boston, MA 02115 USA

[2] Joslin Diabet Ctr, Boston, MA 02115 USA

来源：

JOURNAL OF EXPERIMENTAL MEDICINE | 2003年 / 197卷 / 12期

关键词：

diabetes; NOD mouse; tolerance; GAD65; autoimmunity;

D O I：

10.1084/jem.20030215

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Experiments in nonobese diabetic (NOD) mice that lacked expression of glutamic acid decarboxylase (GAD) in P cells have suggested that GAD represents an autoantigen essential for initiating and maintaining the diabetogenic immune response. Several attempts of inducing GAD-specific recessive tolerance to support this hypothesis have failed. Here we report on successful tolerance induction by expressing a modified form of GAD under control of the invariant chain promoter resulting in efficient epitope display. In spite of specific tolerance insulitis and diabetes occurred with normal kinetics indicating that GAD is not an essential autoantigen in the pathogenesis of diabetes.

引用

收藏

页码：1635 / 1644

页数：10

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