Protection of Nonobese Diabetic Mice from Diabetes by Gene(s) Closely Linked to IFN-γ Receptor Loci

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.