| Project/Area Number |
18K19439
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Review Section |
Medium-sized Section 49:Pathology, infection/immunology, and related fields
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
Ohteki Toshiaki 東京医科歯科大学, 難治疾患研究所, 教授 (50233200)
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| Project Period (FY) |
2018-06-29 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2019: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2018: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 造血幹細胞（HSC） / 貪食 / 死細胞 / ホスファチジルセリン / 造血幹前駆細胞 / 免疫特権領域 / エンドサイトーシス / 抗原提示 |
|---|
| Outline of Final Research Achievements |
We found that surface molecules that are originally expressed on macrophages (MHC class II, F4/80, CD80, CD86, PD-L1 etc.) are also expressed on hematopoietic stem cells (HSCs). Based on this finding, we demonstrated that HSCs phagocytosed dead cell fragments by recognizing phosphatidylserine (PS) expressed on them ex vivo and in vivo. Furthermore, it was suggested that HSCs may accelerate their proliferation and/or survival by recognizing PS.
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| Academic Significance and Societal Importance of the Research Achievements |
これらの研究成果は、HSCが周辺の死細胞断片を認識・貪食することによって、HSC自身の増殖・生存を加速させる可能性を提示している。今後、定常状態だけでなく、死細胞がより多く生じる炎症、放射線照射、抗がん剤投与など、生体ストレス応答時のHSCの解析を行うことで、これまで知らせていなかったHSC自身による造血系恒常性維持機構が明らかになることが期待される。
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