Localization of Idd11 is not associated with thymus and NKT cell abnormalities in NOD mice
Localization of Idd11 is not associated with thymus and NKT cell abnormalities in NOD mice
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DOI：
10.2337/diabetes.54.12.3453
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发表时间：
2005-12-01
期刊：
影响因子：
7.7
通讯作者：
Morahan, G
中科院分区：
文献类型：
--
作者：
Brodnicki, TC;Fletcher, AL;Morahan, G
同源小鼠品系为非肥胖糖尿病（NOD）小鼠中与糖尿病进展相关的染色体区域的遗传解剖和生物学表征提供了独特的资源。idd 11是一个小鼠糖尿病易感基因座，以前定位于4号染色体上的一个区域。比较一组来自非糖尿病C57 BL/6（B6）品系的具有不同间隔的亚同源NOD小鼠品系，现在将Idd 11映射到类似于8 Mb的间隔。即使胰岛的淋巴细胞浸润与NOD小鼠中发现的相似，B6衍生的间隔也能保护同系NOD小鼠免于糖尿病发作。此外，无论是胸腺结构的不规则性，也没有NKT细胞的缺陷，改善糖尿病耐药的同系NOD小鼠，表明Idd 11并不有助于这些异常，不需要纠正，以防止疾病。
Congenic mouse strains provide a unique resource for genetic dissection and biological characterization of chromosomal regions associated with diabetes progression in the nonobese diabetic (NOD) mouse. Idd11, a mouse diabetes susceptibility locus, was previously localized to a region on chromosome 4. Comparison of a panel of subcongenic NOD mouse strains with different intervals derived from the nondiabetic C57BL/6 (B6) strain now maps Idd11 to an similar to 8-Mb interval. B6-derived intervals protected congenic NOD mice from diabetes onset, even though lymphocytic infiltration of pancreatic islets was similar to that found in NOD mice. In addition, neither thymic structural irregularities nor NKT cell deficiencies were ameliorated in diabetes-resistant congenic NOD mice, indicating that Idd11 does not contribute to these abnormalities, which do not need to be corrected to prevent disease.