AOD2, THE LOCUS CONTROLLING DEVELOPMENT OF ATROPHY IN NEONATAL THYMECTOMY-INDUCED AUTOIMMUNE OVARIAN DYSGENESIS, COLOCALIZES WITH IL2, FGFB, AND IDD3

In genetically susceptible strains of mice, such as A/J and (C57BL/6J X A/J)F-1 hybrids, neonatal thymectomy-induced autoimmune ovarian dysg enesis (AOD) is characterized by the development of antiovarian autoan tibodies, oophoritis, and atrophy. Temporally, atrophy may be observed during and after the regression of inflammatory infiltrates from the ovary. Histologically, lesions appear as areas devoid of ovarian folli cles in all stages of development that have been replaced by luteinize d interstitial cells. We report here the mapping of Aod2, the locus th at controls this phenotype, to mouse chromosome 3 within a region enco ding Il2 and Fgfb. Most significant, however, is the co-localization o f Aod2 to Idd3, a susceptibility gene that plays a role in autoimmune insulin-dependent type 1 diabetes mellitus in the nonobese diabetic mo use.