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

Authors
Yoon, JW; Yoon, CS; Lim, HW; Huang, QQ; Kang, Y; Pyun, KH; Hirasawa, K; Sherwin, RS; Jun, HS
Citation
Science, 284(5417):1183-1187, 1999
Journal Title
Science
ISSN
0193-4511
Abstract
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 GAD transgenic NOD mice prevented autoimmune diabetes, whereas persistent GAD expression in the beta 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 beta cell GAD expression blocked the generation of diabetogenic T cells and protected islet grafts from autoimmune injury. Thus, beta 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.
MeSH terms
Adoptive TransferAnimalsAutoantigens/geneticsAutoantigens/immunology*Autoantigens/physiologyAutoimmunityDNA, AntisenseDiabetes Mellitus, Type 1/enzymology*Diabetes Mellitus, Type 1/immunology*Diabetes Mellitus, Type 1/pathologyFemaleGene ExpressionGlutamate Decarboxylase/geneticsGlutamate Decarboxylase/immunology*Glutamate Decarboxylase/physiologyInsulin/bloodInsulin/metabolismIslets of Langerhans/enzymology*Islets of Langerhans/immunologyIslets of Langerhans/metabolismIslets of Langerhans/pathologyIslets of Langerhans TransplantationLymphocyte ActivationMaleMiceMice, Inbred NODMice, SCIDMice, TransgenicT-Lymphocytes/immunologyTransgenes
PMID
10325232
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Endocrinology & Metabolism
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
AJOU Authors
윤, 지원강, 엽
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