| Project/Area Number |
18K07163
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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 49070:Immunology-related
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| Research Institution | Yamagata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
奈良 英利 石巻専修大学, 理工学部, 准教授 (00375338)
武田 裕司 山形大学, 医学部, 准教授 (90302299)
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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: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | IL-12 / ADAM17 / ADAM / サイトカイン / 抗腫瘍免疫 |
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| Outline of Final Research Achievements |
IL-12 is an important cytokine for the induction of Th1 cell-mediated immunity. There are secretory and membrane-bound types of IL-12, and we have reported that membrane-bound IL-12 exhibits stronger Th1 inducibility than the secretory type. Therefore, we thought that regulation of membrane-bound IL-12 expression might promote anti-tumor immunity mediated by Th1 response. To this end, we first attempted to elucidate the secretory mechanism of membrane-bound IL-12, and found that a proteolytic enzyme called ADAM17 may be indirectly involved. Membrane-bound IL-12 is expected to be associated with some molecule that is cleaved by ADAM17 and is currently being searched for that molecule.
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| Academic Significance and Societal Importance of the Research Achievements |
ADAM17は膜結合型TNFαを切断して分泌させる酵素として発見された。これまでに多くの膜分子がADAM17により切断され、機能が調節されることが判明している。IL-12についても、ADAM17が膜結合型から分泌型への変換に関わっていることが示唆された。膜結合型IL-12がどのようなメカニズムでTh1免疫応答を亢進させるのかについて、これまでのところ結論を得ることはできなかったが、今後ADAM17を介した新たな細胞性免疫応答の調節機構となることが期待される。
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