剖析非肥胖糖尿病（NOD）同源近交系小鼠自身免疫的遗传控制。
Dissecting genetic control of autoimmunity in NOD congenic mice.
作者信息
Ridgway William M
机构信息
University of Pittsburgh, Pittsburgh, PA, USA.
出版信息
Immunol Res. 2006;36(1-3):189-95. doi: 10.1385/IR:36:1:189.
Abstract
My lab investigates genetic control of autoimmune disease and autoimmune phenotypes using a series of nonobese diabetic (NOD) congenic mice. NOD congenic mice have regions from B6/B10 introgressed onto the NOD genetic background, which reduces the severity/incidence of autoimmune diabetes. We have demonstrated, however, that while diabetes is reduced, other autoimmune phenotypes and diseases arise in NOD congenic mice. Mapping the genomic regions responsible for these phenotypes has produced novel insights into genetic control of autoimmunity. This review will illustrate some of the genetically controlled phenotypes we have investigated, which shed light upon autoimmune features relevant to human type 1 diabetes, systemic lupus erythematosus, and primary biliary cirrhosis.
摘要
我的实验室使用一系列非肥胖糖尿病（NOD）同源近交系小鼠研究自身免疫性疾病和自身免疫表型的遗传控制。NOD同源近交系小鼠具有从B6/B10导入到NOD遗传背景上的区域，这降低了自身免疫性糖尿病的严重程度/发病率。然而，我们已经证明，虽然糖尿病有所减轻，但NOD同源近交系小鼠中会出现其他自身免疫表型和疾病。对负责这些表型的基因组区域进行定位，为自身免疫的遗传控制带来了新的见解。这篇综述将阐述我们所研究的一些受遗传控制的表型，这些表型揭示了与人类1型糖尿病、系统性红斑狼疮和原发性胆汁性肝硬化相关的自身免疫特征。
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