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

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Title
Control of autoimmune diabetes in NOD mice by GAD expression or suppression in β-cells
Author(s)
Ji Won Yoon; Chang Soon Yoon; Hye Won Lim; Q Q Huang; Yup Kang; Kwang Ho Pyun; K Hirasawa; R S Sherwin; Hee Sook Jun
Bibliographic Citation
Science, vol. 284, no. 5417, pp. 1183-1187
Publication Year
1999
Abstract
Glutamic and decarboxylase (GAD) is a pancreatic β cell autoantigen in humans and nonobese diabetic (NOD) mice. β Cell-specific suppression of GAD expression in two lines of antisense GAD transgenic NOD mice prevented autoimmune diabetes, whereas persistent GAD expression in the β cells in the other four lines of antisense GAD transgenic NOD mice resulted in diabetes, similar to that seen in transgene-negative NOD mice. Complete suppression of β cell GAD expression blocked the generation of diabetogenic T cells and protected islet grafts from autoimmune injury. Thus, β cell-specific GAD 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.
ISSN
0036-8075
Publisher
Amer Assoc Advancement Science
DOI
http://dx.doi.org/10.1126/science.284.5417.1183
Type
Article
Appears in Collections:
1. Journal Articles > Journal Articles
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