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Receptor Loci1
Center for Immunology and Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110
Nonobese diabetic (NOD) mice carrying a segment of chromosome
flanking the disrupted IFN-
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-
R-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-
receptor gene but, rather, is
influenced by the presence of a diabetes-resistant gene(s) closely
linked to the IFN-
R loci derived from the 129 mouse
strain.
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