Yamaji Kaori, Ikegami Hiroshi, Fujisawa Tomomi, Noso Shinsuke, Nojima Koji, Babaya Naru, Itoi-Babaya Michiko, Makino Susumu, Sakamoto Tsutomu, Ogihara Toshio
Department of Geriatric Medicine, Osaka University Graduate School of Medicine, Japan.
Biochem Biophys Res Commun. 2005 Jun 3;331(2):536-42. doi: 10.1016/j.bbrc.2005.04.005.
Among polygenes conferring susceptibility to type 1 diabetes in the NOD mouse, Idd10 on distal chromosome 3 has been shown to be important for disease susceptibility. In this study, we investigated the candidacy of Fcgr1 and Cd101 for Idd10, by congenic mapping and candidate gene sequencing. Among seven NOD-related strains studied, the IIS mouse was found to possess a recombinant Idd10 interval with the same sequence at Fcgr1 as the NOD mouse, but a different sequence at Cd101 from that in the NOD mouse with 10 amino acid substitutions. The frequency of type 1 diabetes in NOD mice congenic for IIS Idd10 (NOD.IISIdd10) was significantly reduced as compared to that in the NOD mouse, despite the presence of the identical Fcgr1 sequence. These data indicate that IIS mice possess a resistant allele at Idd10, and suggest that Cd101, but not Fcgr1, is responsible for the Idd10 effect.
在赋予非肥胖糖尿病（NOD）小鼠1型糖尿病易感性的多基因中，位于3号染色体远端的Idd10已被证明对疾病易感性很重要。在本研究中，我们通过同源定位和候选基因测序研究了Fcgr1和Cd101作为Idd10的候选基因。在所研究的7个与NOD相关的品系中，发现IIS小鼠具有重组的Idd10区间，其Fcgr1序列与NOD小鼠相同，但Cd101序列与NOD小鼠不同，有10个氨基酸替换。尽管存在相同的Fcgr1序列，但与NOD小鼠相比，携带IIS Idd10的同源基因NOD小鼠（NOD.IISIdd10）的1型糖尿病发病率显著降低。这些数据表明IIS小鼠在Idd10处具有抗性等位基因，并提示Cd101而非Fcgr1是Idd10效应的原因。
