非肥胖糖尿病（NOD）Idd9基因区间影响胰岛炎的致病性，并且包含Cd30、Tnfr2和Cd137的分子变体。
The NOD Idd9 genetic interval influences the pathogenicity of insulitis and contains molecular variants of Cd30, Tnfr2, and Cd137.
作者信息
Lyons P A, Hancock W W, Denny P, Lord C J, Hill N J, Armitage N, Siegmund T, Todd J A, Phillips M S, Hess J F, Chen S L, Fischer P A, Peterson L B, Wicker L S
机构信息
The Wellcome Trust Centre for Molecular Mechanisms in Disease, Cambridge University, United Kingdom.
出版信息
Immunity. 2000 Jul;13(1):107-15. doi: 10.1016/s1074-7613(00)00012-1.
Previous analyses of NOD mice have shown that some genes control the development of both insulitis and diabetes, while other loci influence diabetes without reducing insulitis. Evidence for the existence of a gene only influencing diabetes, Idd9 on mouse chromosome 4, is provided here by the development of a novel congenic mouse strain, NOD.B10 Idd9. NOD.B10 Idd9 mice display profound resistance to diabetes even though nearly all develop insulitis. Subcongenic analysis has demonstrated that alleles of at least three B10 genes, Idd9.1, Idd9.2, and Idd9.3 are required to produce Idd9-mediated diabetes resistance. Candidate genes with amino acid differences between the NOD and B10 strains have been localized to the 5.6 cM Idd9.2 interval (Tnfr2, Cd30) and to the 2.0 cM Idd9.3 interval (Cd137).
先前对非肥胖糖尿病（NOD）小鼠的分析表明，一些基因控制胰岛炎和糖尿病的发展，而其他基因座影响糖尿病但不减轻胰岛炎。本文通过培育一种新型同源近交系小鼠NOD.B10 Idd9，提供了仅影响糖尿病的基因（位于小鼠4号染色体上的Idd9）存在的证据。NOD.B10 Idd9小鼠对糖尿病具有显著抗性，尽管几乎所有小鼠都会发展为胰岛炎。亚同源近交分析表明，至少三个B10基因Idd9.1、Idd9.2和Idd9.3的等位基因是产生Idd9介导的糖尿病抗性所必需的。在NOD和B10品系之间存在氨基酸差异的候选基因已定位到5.6 cM的Idd9.2区间（Tnfr2、Cd30）和2.0 cM的Idd9.3区间（Cd137）。
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