| Project/Area Number |
26293400
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
Nagai Shigenori 東京医科歯科大学, 医歯(薬)学総合研究科, 准教授 (50348801)
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| Co-Investigator(Kenkyū-buntansha) |
東 みゆき 東京医科歯科大学, 医歯(薬)学総合研究科, 教授 (90255654)
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| Co-Investigator(Renkei-kenkyūsha) |
YOSHIMURA Akihiko 慶應義塾大学, 医学部, 教授 (90182815)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥16,120,000 (Direct Cost: ¥12,400,000、Indirect Cost: ¥3,720,000)
Fiscal Year 2016: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2015: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
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| Keywords | IL-10 / ヘルパーT細胞 / PI3K / 免疫学 / 細菌感染 / 粘膜免疫 |
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| Outline of Final Research Achievements |
Since Foxp3-negative, IL-10-producing regulatory T (Tr1) cells are quite important for the suppression of chronic inflammation, I tried to investigate the regulatory mechanisms of Tr1 differentiation. When I added the inhibitor of PI3K, a kind of lipid kinases, in Tr1 differentiation by IL-27, I was able to suppress Tr1 differentiation. In contrast, Tr1 differentiation was enhanced when the PI3K pathway was augmented. These results suggest that PI3K pathway positively regulates the differentiation of IL-27-induced Tr1 cells.
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