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

Ji Won Yoon*, Chang Soon Yoon, Hye Won Lim, Qi Quan Huang, Yup Kang, Kwang Ho Pyun, Kensuke Hirasawa, Robert S. Sherwin, Hee Sook Jun

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

232 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1183-1187
Number of pages5
JournalScience
Volume284
Issue number5417
DOIs
StatePublished - May 14 1999

ASJC Scopus subject areas

  • General

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