Molecular mechanisms on antigen presenting cell function and generation

2022 Fiscal Year Final Research Report

• Project/Area Number: 20H03505
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Review Section: Basic Section 49070:Immunology-related
• Research Institution: Wakayama Medical University
• Principal Investigator: Kaisho Tsuneyasu 和歌山県立医科大学, 先端医学研究所, 教授 (60224325)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 樹状細胞 / 炎症 / 遺伝子改変マウス

Outline of Final Research Achievements

By establishing and analyzing mouse models of autoinflammatory diseases, we attempted to elucidate the molecular mechanisms for regulating antigen-presenting cell function and differentiation. By analyzing the gene variants of COPA, a functional molecule involved in the protein transport, we clarified the novel pathological mechanisms leading to overproduction of type I interferon (IFN) from DNA sensor-stimulated dendritic cells (DCs). By analyzing the gene variants of beta1i subunit of the proteasome, a protein complex that degrades unnecessary or misfolded proteins, proteasome dysfunction can cause defects in DC generation.

Free Research Field

免疫学

Academic Significance and Societal Importance of the Research Achievements

自己炎症性疾患患者の遺伝子バリアントをマウスに導入することにより、ヒトの病態をマウスで再現すると共に、抗原提示細胞の機能や分化に異常を来す病態が明らかになった。本研究により、自己炎症性疾患ばかりでなく、様々な炎症病態の解明が進み、新たな炎症制御剤が見出されることが期待される。