Identification of susceptibility genes for autoimmunity and beta-cell specificity of type 1 diabetes

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K09404
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Metabolomics
• Research Institution: Kindai University
• Principal Investigator: IKEGAMI Hiroshi 近畿大学, 医学部, 教授 (20221062)
• Co-Investigator(Kenkyū-buntansha): 馬場谷 成 近畿大学, 医学部, 講師 (10449837) ; 廣峰 義久 近畿大学, 医学部, 講師 (30460851) ; 川畑 由美子 近畿大学, 医学部, 准教授 (80423185) ; 能宗 伸輔 近畿大学, 医学部, 講師 (90460849)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: １型糖尿病 / 自己免疫 / 遺伝子 / 疾患感受性 / 臓器特異性

Outline of Final Research Achievements

The purpose of this study was to identify genes responsible for both autoimmuninty and organ-specificity of type 1 diabetes. Type 1 diabetes and autoimmune thyroid diseases (AITD), alopecia areata and AITD, are often develop in the same individuals, whereas type 1 diabetes and AA are very rare to be observed in the same individuals. HLA-DR4 haplotype (DRB1*04:05-DQB1*04:01) was found to be responsible for beta-cell specificity in autoimmune diseases. targeted disruption of MafA in NOD mice resulted in protection, but not accerelation, of beta-cell autoimmunity and type 1 diabetes. Accumulation of regulatory T-cells in insulitis legion was suggested to be possible mechanism of protection from beta-cell autoimmunity and type 1 diabetes.

Free Research Field

内分泌・代謝・糖尿病学、分子遺伝学、免疫学