Control of autoimmune diabetes in NOD mice by CAD expression or suppression in β cells

被引：210

作者：

Yoon, JW ^{[1
]}

Yoon, CS

Lim, HW

Huang, QQ

Kang, Y

Pyun, KH

Hirasawa, K

Sherwin, RS

Jun, HS

机构：

[1] Univ Calgary, Fac Med, Julia McFarlane Diabet Res Ctr, Lab Viral & Immunopathogenesis Diabet, Calgary, AB T2N 4N1, Canada

[2] Univ Calgary, Fac Med, Dept Microbiol & Infect Dis, Calgary, AB T2N 4N1, Canada

[3] Ajou Univ, Sch Med, Dept Endocrinol & Metab, Lab Endocrinol,Inst Med Sci, Suwon 442749, South Korea

[4] Yale Univ, Sch Med, Diabet Endocrinol Res Ctr, New Haven, CT 06520 USA

[5] Korea Res Inst Biosci & Biotechnol, Taejon 305333, South Korea

来源：

SCIENCE | 1999年 / 284卷 / 5417期

关键词：

D O I：

10.1126/science.284.5417.1183

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Glutamic acid decarboxylase (GAD) is a pancreatic beta cell autoantigen in humans and nonobese diabetic (NOD) mice. beta Cell-specific suppression of GAD expression in two Lines of antisense CAD transgenic NOD mice prevented autoimmune diabetes, whereas persistent GAD expression in the beta cells in the other four Lines of antisense CAD transgenic NOD mice resulted in diabetes, similar to that seen in transgene-negative NOD mice. Complete suppression of beta cell GAD expression blocked the generation of diabetogenic T cells and protected islet grafts from autoimmune injury. Thus, beta cell-specific CAD expression is required for the development of autoimmune diabetes in NOD mice, and modulation of GAD might, therefore, have therapeutic value in type 1 diabetes.

引用

页码：1183 / 1187

页数：5

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