| Project/Area Number |
25460363
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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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| Research Field |
General medical chemistry
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| Research Institution | Keio University (2015)
Kyoto University (2013-2014) |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
MIYACHI Hitoshi 京都大学, ウイルス研究所, 技術専門職員 (90599200)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 免疫寛容 / 自己免疫 / がん免疫 / 抑制レセプター / Ｔ細胞 / 抑制受容体 / PD-1 / T細胞 / 遺伝子改変マウス / 免疫疲弊 / 新規マウスモデル |
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| Outline of Final Research Achievements |
PD-1 is induced on activated lymphocytes, inhibits their excessive activation, and thereby prevents damage on self-tissues. In durable immune reaction, for example, chronic infection and cancer, PD-1 is super-strongly expressed, which prevents useful immune reaction. The mechanism of the strong PD-1 expression was unclear. In this study, I aimed to determine what causes strong PD-1 expression in vivo. (1) I utilized molecular genetic tools to create a reporter mice that allows faithful detection of PD-1 expression in mice. (2) I found that IL-7, a homeostatic cytokine for lymphocytes negatively regulates PD-1 expression. In a separate line of experiment, I showed PD-1 controls innate immune reaction by inhibiting macrophage activation. The current study will bring a useful information to understand the biology of PD-1.
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