| Project/Area Number |
17K17108
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | Keio University |
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Principal Investigator |
FUJITA KOHEI 慶應義塾大学, 医学部(信濃町), 講師(非常勤) (80624634)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2019: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2018: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | ADAM10 / シェディング / FLT3L / 樹状細胞 / Flt3L / 免疫学 / 酵素 / 炎症 |
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| Outline of Final Research Achievements |
The purpose of this study was to clarify the immunological mechanism of the ADAM10(A disintegrin and metalloproteinase).Analysis of dendritic cell (DC) specific ADAM10 deficient mice suggested that ADAM10 is essential for conventional DC2 differentiation in the spleen.Furthermore, in the analysis of this mouse, the FLT3L concentration in peripheral blood was decreased.From these results, the experiment of culturing fibroblasts in which ADAM10 was specifically deleted in mouse fibroblasts was conducted, and it was shown that cDC2 is a new source of Flt3L.
These results suggest that FLT3L may be involved in the differentiation of DC through ADAM10.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究により、獲得免疫の要となる樹状細胞の臓器特異的な一つの分化機構の可能性を示し、FLT3Lの新たな産生細胞の発見、ADAM10による免疫調整機構の発見により、今後の樹状細胞の研究に新たな方向性を見出した。特にcDC2は液性免疫の中心となるCD4 +T細胞の分化を誘導する細胞であり、局所におけるB細胞い機能や抗体の産生能などへの影響をさらに解析することで免疫疾患への新たなアプローチや炎症制御、ワクチン開発、腫瘍免疫の治療戦略の基盤として役立つこと期待している。
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