Prevention of diabetes in non-obese diabetic I-Ak transgenic mice
Autor: | Thomas E. Mandel, Jacques F. A. P. Miller, Brett Charlton, Janette Allison, Robyn M. Slattery, Lars Kjer-Nielsen |
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Rok vydání: | 1990 |
Předmět: |
Genetically modified mouse
CD4-Positive T-Lymphocytes medicine.medical_specialty Adoptive cell transfer T-Lymphocytes Fluorescent Antibody Technique Gene Expression Mice Transgenic Nod Biology Major histocompatibility complex Diabetes Mellitus Experimental Islets of Langerhans Mice Diabetes mellitus Internal medicine medicine Animals Tissue Distribution NOD mice Multidisciplinary Histocompatibility Antigens Class II Immunization Passive medicine.disease Mononuclear cell infiltration Endocrinology Diabetes Mellitus Type 1 Immunology biology.protein Insulitis |
Zdroj: | Nature. 345(6277) |
ISSN: | 0028-0836 |
Popis: | The non-obese diabetic (NOD) mouse develops insulin-dependent diabetes mellitus (IDDM) with mononuclear cell infiltration of the islets of Langerhans and selective destruction of the insulin-producing beta-cells, as in humans. Most infiltrating cells are T lymphocytes, and most of these carry the CD4 antigen. Adoptive transfer of T cells from diabetic NOD mice into irradiated NOD or athymic nude NOD mice induces diabetes. Susceptibility to IDDM in NOD mice is polygenic, with one gene linked to the major histocompatibility complex class II locus, which in NOD mice expresses a unique I-A molecule but no I-E. Speculation exists as to the role of the I-A molecule in the diabetes susceptibility of NOD mice, especially regarding the significance of specific unique residues. To examine the role of the NOD I-A molecule in IDDM pathogenesis, we made NOD/Lt mice transgenic for I-Ak by microinjecting I-Ak alpha- and beta-genes into fertilized NOD/Lt eggs. Insulitis was markedly reduced and diabetes prevented in NOD/Lt mice expressing I-Ak. |
Databáze: | OpenAIRE |
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