| Project/Area Number |
18K14598
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 42020:Veterinary medical science-related
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| Research Institution | Rakuno Gakuen University (2021-2022)
Osaka Ohtani University (2018-2020) |
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Principal Investigator |
Moriya Taiki 酪農学園大学, 獣医学群, 講師 (30759759)
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| Project Period (FY) |
2018-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | CD103+樹状細胞 / 腫瘍免疫 / KiKGR / XCR1 / XCL1 / XCR1樹状細胞 / KikGRマウス / KikGR / フローサイトメトリー / Fucciマウス / 腫瘍浸潤樹状細胞 |
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| Outline of Final Research Achievements |
CD103+ dendritic cells (cDC1) are important for antigen presentation to anti-tumor CD8+T cells. Initially, we attempted to detect molecules that are specifically expressed on the tumor remaining cDC1 but were unable to identify them. However, when tumor cells that overexpressing XCL1, a ligand for XCR1, a chemokine receptor specifically expressed on cDC1, were inoculated, we found enhancement of cDC1 infiltration in the tumor and CD8+ T cell proliferation in the tumor-draining lymph nodes (tdLNs), the site of antigen presentation. These results suggested that enhancement of cDC1 infiltration into the tumor may lead to enhanced anti-tumor immune response through the promotion of the induction of anti-tumor CD8+T cells in the tdLNs.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究遂行により、当初目標とした抗腫瘍CD8+T細胞の誘導に重要なcDC1が腫瘍に留まるために利用する分子の同定には至らなかったが、腫瘍内XCL1増加によりcDC1の腫瘍浸潤が増強し,腫瘍所属リンパ節内でのCD8+T細胞の増加につながる可能性が示された。XCL1-XCR1ケモカインシステムはマウス、ヒトのみならず、イヌなどその他の種にも存在することから、医学、獣医学領域でのより効率的な抗腫瘍CD8+T細胞の誘導を介した免疫療法の開発、改善のための重要な知見となると考えている。
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