Abstract
Nonobese diabetic (NOD) mice carrying a segment of chromosome flanking the disrupted IFN-gamma receptor gene from original 129 ES cells are resistant to development of diabetes. However, extended backcrossing of this mouse line to the NOD mouse resulted in a segregation of the IFN-gammaR-deficient genotype from the diabetes-resistant phenotype. These results indicate that the protection of NOD mice from the development of diabetes is not directly linked to the defective IFN-gamma receptor gene but, rather, is influenced by the presence of a diabetes-resistant gene(s) closely linked to the IFN-gammaR loci derived from the 129 mouse strain.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adoptive Transfer
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Animals
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Diabetes Mellitus, Type 1 / genetics*
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Diabetes Mellitus, Type 1 / immunology
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Diabetes Mellitus, Type 1 / pathology
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Diabetes Mellitus, Type 1 / prevention & control*
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Female
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Genetic Linkage / immunology*
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Genetic Markers / immunology
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Genetic Predisposition to Disease / etiology
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Genetic Predisposition to Disease / genetics*
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Genotype
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Histocompatibility Antigens Class I / biosynthesis
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Immunity, Innate / genetics
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Interferon gamma Receptor
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Interferon-gamma* / metabolism
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Interferon-gamma* / pharmacology
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Islets of Langerhans / pathology
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Macrophages, Peritoneal / immunology
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Macrophages, Peritoneal / metabolism
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Mice
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Mice, Inbred NOD
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Mice, Knockout
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Receptors, Interferon / biosynthesis
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Receptors, Interferon / genetics*
Substances
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Genetic Markers
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Histocompatibility Antigens Class I
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Receptors, Interferon
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Interferon-gamma