| Project/Area Number |
18K08262
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 53050:Dermatology-related
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
藤村 卓 東北大学, 大学病院, 講師 (50396496)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥260,000 (Direct Cost: ¥200,000、Indirect Cost: ¥60,000)
Fiscal Year 2019: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2018: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | IL-36β / 悪性黒色腫 / PD-1 / サイトカイン / 血管新生 / 腫瘍免疫 / 免疫遺伝子治療 |
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| Outline of Final Research Achievements |
IL-36β is produced by bronchial epithelial cells and dendritic cells. To examine the anti-tumor activity of IL-36 β, we constructed two types of recombinant retroviral vector DFG-PTH-truncated IL-36β-IRES-Neo and DFG-GH-truncated IL-36β-IRES-Neocarrying truncated IL-36β, and transduced into B16-F10 melanoma cells. Established B16-F10-PTH-truncated IL-36β cells and B16-F10-GH-truncated IL-36β cells grew very slowly compared with that of parental B16-F10 cells in vivo. We examined the mechanisms of anti-tumor effects of truncated IL-36β, and found that truncated IL-36β could down-regulate the surface expression levels of programmed cell death (PD)-1 on CD4 and CD8 T cells stimulated by anti-CD3 monoclonal antibody and anti-CD28 monoclonal antibody.
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| Academic Significance and Societal Importance of the Research Achievements |
IL-36β は抗癌作用を有しており、その抗癌機序として CD4 および CD8 T 細胞上の免疫チェックポイント分子 PD-1 の発現を低下させる作用が関与している可能性が示唆された。
今後 IL-36β が CD4 および CD8 T 細胞上の PD-1 の発現を低下させる作用の機序を解明すれば、新たな公害材の開発につながる可能性がある。
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