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2023 Fiscal Year Final Research Report

Exploring the relationship between changes in cellular metabolism within the pancreatic islet environment and the progression of autoimmune diabetes

Research Project

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Project/Area Number 21K08558
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 InstitutionNagasaki University

Principal Investigator

Niri Tetsuro  長崎大学, 医歯薬学総合研究科(医学系), 助教 (10782550)

Co-Investigator(Kenkyū-buntansha) 阿比留 教生  長崎大学, 医歯薬学総合研究科(医学系), 客員研究員 (00380981)
赤澤 諭  長崎大学, 原爆後障害医療研究所, 助教 (50549409)
Project Period (FY) 2021-04-01 – 2024-03-31
KeywordsNODマウス / 1型糖尿病 / 膵島自己免疫
Outline of Final Research Achievements

In adoptive transfer experiments using CD4+ T cells harvested from IRF4-deficient BDC2.5Tg NOD mice, analysis of the islet-infiltrating cells of adoptively transferred recipients revealed new insights into IRF4 dose-dependent T cell proliferation and promotion of differentiation into Th1/Th17 double-positive cells. Furthermore, in vitro stimulation experiments with strong antigens showed a slight decrease in T-cell proliferation capacity in the IRF4-deficient group, although extreme cell proliferation and T-cell differentiation dependent on IRF4 dosage were not observed. Additionally, under TCR stimulation conditions, the aerobic glycolysis capability of IRF4-deficient CD4+ T cells was reduced.

Free Research Field

内分泌・代謝学

Academic Significance and Societal Importance of the Research Achievements

抗原特異的BDC2.5 CD4+ T細胞におけるIRF4発現用量依存性の糖尿病進展形成の要因として、活性化T細胞の機能変化と、解糖系優位の代謝変化の関連性が示唆された。IRF4発現調整そのものを目的とした治療は、広範な免疫不全などの副作用が危惧される。しかし、今回我々が示したT細胞代謝活性化の抑制など、IRF4関連の免疫細胞を標的とした1型糖尿病治療開発や、T細胞マーカーとしてのIRF4発現モニタリングによる機能的T細胞診断など、今後の臨床応用への展望が期待される。

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Published: 2025-01-30  

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