Protection of nonobese diabetic mice from diabetes by gene (s) closely linked to IFN-γ receptor loci
O Kanagawa, G Xu, A Tevaarwerk… - The Journal of …, 2000 - journals.aai.org
O Kanagawa, G Xu, A Tevaarwerk, BA Vaupel
The Journal of Immunology, 2000•journals.aai.orgNonobese diabetic (NOD) mice carrying a segment of chromosome flanking the disrupted
IFN-γ 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-γR-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-γ receptor gene but, rather, is influenced by the presence …
IFN-γ 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-γR-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-γ receptor gene but, rather, is influenced by the presence …
Abstract
Nonobese diabetic (NOD) mice carrying a segment of chromosome flanking the disrupted IFN-γ 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-γR-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-γ receptor gene but, rather, is influenced by the presence of a diabetes-resistant gene (s) closely linked to the IFN-γR loci derived from the 129 mouse strain.
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