| Literature DB >> 10725755 |
O Kanagawa1, G Xu, A Tevaarwerk, B A Vaupel.
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.Entities:
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Year: 2000 PMID: 10725755 DOI: 10.4049/jimmunol.164.7.3919
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422