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Insulin-dependent diabetes in NOD mice and mouse experimental autoimmune encephalomyelitis (EAE) are the major disease models for human type I diabetes and multiple sclerosis, respectively. In recent genetic analyses, a number of quantitative trait loci (QTL) controlling susceptibility to these autoimmune diseases have been identified1, 2, 3, 4. Some QTL overlap between the two diseases, raising the possibility that there may be disease genes common to diabetes and EAE (5). Given the large number of QTL identified and the large QTL support interval sizes attained in the genetic segregation analyses used, we investigated whether this overlap was due to a shared 'autoimmunity gene' or merely to the coincidental grouping of two unrelated genes. Among the diabetes QTL mapped so far in NOD mice, two overlap with QTL that we identified in EAE (1). One of these QTL, in the medial region of chromosome 3, has been further analysed through the generation of congenic mice and was found to be composed of QTL Idd3, Idd17, Idd10 and Idd18 (refs 6,7). We were able to more precisely examine the effect of the diabetes QTL on EAE using these NOD congenic lines, which carry diabetes-resistance alleles at one or more of these QTL (refs 6,7).

Original publication




Journal article


Nature genetics

Publication Date





158 - 160


Animals, Mice, Congenic, Mice, Inbred C57BL, Mice, Inbred NOD, Mice, Encephalomyelitis, Autoimmune, Experimental, Diabetes Mellitus, Type 1, Interleukin-2, Chromosome Mapping, Amino Acid Sequence, Quantitative Trait, Heritable, Molecular Sequence Data