Control of Autoimmune Diabetes in NOD Mice by GAD Expression or Suppression in β Cells
| Autor: | Chang Soon Yoon, Qi Quan Huang, Robert S. Sherwin, Hee-Sook Jun, Ji-Won Yoon, K. Hirasawa, Hye Won Lim, Kwang Ho Pyun, Yup Kang |
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| Rok vydání: | 1999 |
| Předmět: |
Male
endocrine system medicine.medical_specialty endocrine system diseases T-Lymphocytes Glutamate decarboxylase Islets of Langerhans Transplantation Gene Expression Autoimmunity Mice Transgenic Mice SCID Nod Biology Lymphocyte Activation medicine.disease_cause Autoantigens DNA Antisense Islets of Langerhans Mice Mice Inbred NOD Internal medicine medicine Animals Insulin Transgenes B cell NOD mice Autoimmune disease Type 1 diabetes Multidisciplinary Glutamate Decarboxylase nutritional and metabolic diseases medicine.disease Adoptive Transfer Diabetes Mellitus Type 1 medicine.anatomical_structure Endocrinology Immunology Female Beta cell |
| Zdroj: | Science. 284:1183-1187 |
| ISSN: | 1095-9203 0036-8075 |
| DOI: | 10.1126/science.284.5417.1183 |
| Popis: | Glutamic acid 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. |
| Databáze: | OpenAIRE |
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