| Project/Area Number |
25670234
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Immunology
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| Research Institution | Keio University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
YAMADA Satoshi 岡山理科大学, 工学部, 教授 (20393506)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | サイトカイン / シグナル伝達 / 転写因子 / ヘルパーT細胞 / 制御性T細胞 / TGFβ / モデル化 / エピジェネティクス / 遺伝子発現制御 |
|---|
| Outline of Final Research Achievements |
Helper T cells have been thought to play a central role in not only acquired immune responses but also in immune regulation. Recently, several subsets such as Th9, Th17 and iTreg have been discovered in addition to Th1 and Th2. Differentiation of each helper T cell subset is extremely complicated. Thus, we have tried to define the mechanism of helper T cell differentiation by focusing on TGF-beta signaling. We discovered Th9 differentiation by TGF-beta and IL-4 is Smad2/3 dependent and required for IRF4 transcription factor. We also found that TGF-beta from dendritic cells plays important role in iTreg differentiation in the gut. We showed that the TLR2-AP-1 pathway as well as the Smad3 pathway are critical for TGF-beta production by intestinal microflora.
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