Aod2是控制新生期胸腺切除诱导的自身免疫性卵巢发育不全中萎缩发育的基因座，它与Il2、Fgfb和Idd3共定位。
Aod2, the locus controlling development of atrophy in neonatal thymectomy-induced autoimmune ovarian dysgenesis, co-localizes with Il2, Fgfb, and Idd3.
作者信息
Teuscher C, Wardell B B, Lunceford J K, Michael S D, Tung K S
机构信息
Department of Microbiology, Brigham Young University, Provo, Utah 84602, USA.
出版信息
J Exp Med. 1996 Feb 1;183(2):631-7. doi: 10.1084/jem.183.2.631.
Abstract
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 Histologically, lesions appear as areas devoid of ovarian follicles in all stages of development that have been replaced by luteinized interstitial cells.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.
摘要
在基因易感性小鼠品系中，如A/J和（C57BL/6J×A/J）F1杂交种，新生期胸腺切除诱导的自身免疫性卵巢发育不全（AOD）的特征是抗卵巢自身抗体的产生、卵巢炎和萎缩。在时间上，萎缩可在卵巢炎症浸润消退期间及之后观察到。组织学上，病变表现为所有发育阶段缺乏卵巢卵泡的区域，这些区域已被黄体化的间质细胞取代。我们在此报告将控制此表型的基因座Aod2定位到小鼠3号染色体上一个编码Il2和Fgfb的区域内。然而，最显著的是Aod2与Idd3共定位，Idd3是一个在非肥胖糖尿病小鼠的自身免疫性胰岛素依赖型1型糖尿病中起作用的易感基因。
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