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2023 Fiscal Year Final Research Report

Basic research for the development of islet-specific dendritic cell vaccination for type 1 diabetes

Research Project

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Project/Area Number 21K08525
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 54040:Metabolism and endocrinology-related
Research InstitutionUniversity of Toyama

Principal Investigator

Chujo Daisuke  富山大学, 学術研究部医学系, 教授 (30640528)

Co-Investigator(Kenkyū-buntansha) 戸邉 一之  富山大学, 学術研究部医学系, 教授 (30251242)
Project Period (FY) 2021-04-01 – 2024-03-31
Keywords1型糖尿病 / 自己免疫 / T細胞
Outline of Final Research Achievements

The aim of this study was to identify responsible islet antigen-specific T cell epitopes in Japanese patients with type 1 diabetes (T1D), and to regulate the pathogenic T cells by using regulatory dendritic cells educated with responsible epitopes. In our analyses, we identified GAD65: 115-127, GAD65: 247-266, Preproinslun: C19-A3, and Preproinsulin: C22-A5 as responsible T cell epitopes in Japanese T1D patients. Furthermore, the frequencies of GAD65: 247-266-specific Th1 cells were significantly higher than those specific for other responsible epitopes. Based on these results, we established the assay to regulate the pathogenic T cell responses by using autologous regulatory dendritic cells educated with GAD65: 247-266.

Free Research Field

糖尿病・代謝学

Academic Significance and Societal Importance of the Research Achievements

1型糖尿病はインスリンを産生する膵島細胞が自己免疫によって破壊され、自身のインスリンが分泌されなくなる難治性疾患である。本研究では、自己免疫の中心的役割を担う、すなわち膵島細胞の破壊を司る免疫細胞(病原性T細胞)を活性化させる引き金を同定した。この引き金と体内の細胞を上手く利用し、1型糖尿病の発症に関わる自己免疫反応を抑えることが可能かどうかについても研究を続けており、これが可能になれば自己免疫による膵島細胞の破壊を防ぐような新しい治療法の開発につながる可能性がある。

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Published: 2025-01-30  

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