| Project/Area Number |
20K09429
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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 56020:Orthopedics-related
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Omata Yasunori 東京大学, 医学部附属病院, 特任准教授 (40570734)
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| Co-Investigator(Kenkyū-buntansha) |
矢野 文子 東京大学, 医学部附属病院, 届出研究員 (80529040)
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| Project Period (FY) |
2020-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2022: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2021: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2020: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 自然免疫細胞 / 破骨細胞 / 自然免疫 |
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| Outline of Research at the Start |
本研究ではヒト及びマウス由来の自然免疫細胞及び破骨細胞に対して最新のシングルセルRNA解析を導入し、様々なサブタイプの免疫細胞が正常な骨代謝をどのように制御するかを、破骨細胞にフォーカスして解析する。さらに骨粗鬆症や関節炎等の病的環境下においても免疫細胞による破骨細胞の制御機構を解析する。シングルセルRNA解析により均一化された細胞集団を抽出することで、特異的なサブセットによる骨代謝制御機構の解明を目指す。
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| Outline of Final Research Achievements |
While the role of T cells in the regulation of bone homeostasis is well defined, little is known about the role of innate lymphoid cells (ILCs) on bone. ILCs are innate immune cells that share cytokine expression patterns with T cells but lack the T cell receptor. In this study we show that type 2 ILCs (ILC2) potently inhibit the generation of bone resorbing osteoclasts in vitro as well as favorably influence bone homeostasis under steady state conditions in vivo using loss and gain of function models. Furthermore, adoptive transfer of ILC2 completely abrogated ovariectomy-induced bone loss by significantly down-regulating osteoclast numbers in vivo.
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| Academic Significance and Societal Importance of the Research Achievements |
In this study we show that type 2 ILCs (ILC2) potently inhibit the generation of bone resorbing osteoclasts in vitro as well as favorably influence bone homeostasis under steady state conditions in vivo using loss and gain of function models. The new insight will uncover the bone and immune biology.
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