Aod2, the locus controlling development of atrophy in neonatal thymectomy-induced autoimmune ovarian dysgenesis, co-localizes with Il2, Fgfb, and Idd3

• Published in: The Journal of experimental medicine Vol. 183; no. 2; pp. 631 - 637
• Main Authors: Teuscher, C, Wardell, B B, Lunceford, J K, Michael, S D, Tung, K S
• Format: Journal Article
• Language: English
• Published: United States The Rockefeller University Press 01.02.1996
• Subjects: Animals; Animals, Newborn; Atrophy; Autoimmune Diseases - etiology; Autoimmune Diseases - genetics; Chromosome Mapping; Diabetes Mellitus, Type 1 - genetics; Female; Fibroblast Growth Factor 2 - genetics; Genetic Linkage; Gonadal Dysgenesis - genetics; Gonadal Dysgenesis - immunology; Interleukin-2 - genetics; Male; Mice; Oophoritis - genetics; Ovarian Diseases - etiology; Ovarian Diseases - genetics; Ovary - abnormalities; Phenotype; Proteins - genetics; Thymectomy
• ISSN: 0022-1007; 1540-9538
• DOI: 10.1084/jem.183.2.631

In genetically susceptible strains of mice, such as A/J and (C57BL/6J x A/J)F1 hybrids, neonatal thymectomy-induced autoimmune ovarian dysgenesis (AOD) is characterized by the development of antiovarian autoantibodies, 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 Histologically, lesions appear as areas devoid of ovarian follicles in all stages of development that have been replaced by luteinized interstitial cells. We report here the mapping of Aod2, the locus that controls this phenotype, to mouse chromosomes 3 within a region encoding Il2 and Fgfb. Most significant, however, is the co-localization of Aod2 to Idd3, a susceptibility gene that plays a role in autoimmune insulin-dependent type 1 diabetes mellitus in the nonobese diabetic mouse.