Development of new cancer immunotherapy that targets the CD69-Myl9/12 system
Project/Area Number |
18K07257
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 50020:Tumor diagnostics and therapeutics-related
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Research Institution | Chiba University |
Principal Investigator |
Nasu Ryo 千葉大学, 大学院医学研究院, 特任助教 (30466859)
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Co-Investigator(Kenkyū-buntansha) |
岩立 康男 千葉大学, 大学院医学研究院, 教授 (70272309)
本橋 新一郎 千葉大学, 大学院医学研究院, 教授 (60345022)
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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 |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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Keywords | がん免疫 / CD69 / 細胞傷害性T細胞 / 免疫チェックポイント阻害剤 / 免疫逃避機構 |
Outline of Final Research Achievements |
The purpose of this study is to develop a new cancer immunotherapy that targets the CD69-Myl9/12 system. Myl12-deficient cancer cells showed reduced tumorigenicity, suggesting an immune evasion by cancer cell-derived Myl9/12. On the other hand, CD69-deficient mice showed increased frequency of cytotoxic differentiated CD8T cells in the tumor microenvironment. Thus, the CD69-Myl9/12 system promotes cancer immune evasion by controlling differentiation of intratumoral CD8T cells.
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Academic Significance and Societal Importance of the Research Achievements |
本研究では、これまでに抗腫瘍免疫応答への関与が着目されていなかったCD69-Myl9/12システムに焦点を当てている。Myl9/12は我々が独自に見出したCD69の機能的リガンドであり、国内外を通じて類似の研究はなく、独自の独創的な研究である。さらに、Myl9/12の放出はがん細胞自体に依存していると考えられるため、抗Myl9/12抗体投与は腫瘍組織を選択的に標的とする、副作用の少ない治療法になる可能性がある。今後、我々の知見からCD69-Myl9/12システムを標的とした新規がん免疫療法が開発され、がん治療に新しい局面が拓かれることを期待している。
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Report
(4 results)
Research Products
(18 results)
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[Journal Article] ACC1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis2019
Author(s)
Yusuke Endo, Atsushi Onodera, Kazushige Obata-Ninomiya, Ryo Koyama-Nasu, Hikari K. Asou, Toshihiro Ito, Takeshi Yamamoto, Toshio Kanno, Takahiro Nakajima, Kenji Ishiwata, Hirotaka Kanuka, Damon J. Tumes, Toshinori Nakayama
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Journal Title
Nature Metabolism
Volume: 1(2)
Issue: 2
Pages: 261-275
DOI
Related Report
Peer Reviewed / Int'l Joint Research
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[Journal Article] SIRT2-mediated inactivation of p73 is required for glioblastoma tumorigenicity2018
Author(s)
Funato K, Hayashi T, Echizen K, Negishi L, Shimizu N, Koyama-Nasu R, Nasu-Nishimura Y, Morishita Y, Tabar V, Todo T, Ino Y, Mukasa A, Saito N & Akiyama T.
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Journal Title
EMBO Reports
Volume: 19
Issue: 11
Pages: 45587-45587
DOI
Related Report
Peer Reviewed / Open Access
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[Presentation] CD1d expression in glioblastoma is a promising target for NKT cell- based cancer immunotherapy2019
Author(s)
Hara, A., Nasu, R., Takami, M., Hirono, S., Matsutani, T., Nakayama, T., Iwadate, Y., Motohashi, S.
Organizer
第78回日本癌学会学術総会
Related Report
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[Presentation] CD1d expression in glioblastoma is a promising target for NKT cell- based cancer immunotherapy2019
Author(s)
Hara, A., Nasu, R., Takami, M., Hirono, S., Matsutani, T., Nakayama, T., Iwadate, Y., Motohashi, S.
Organizer
EMBO workshop CD1-MR1
Related Report
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