| Project/Area Number |
23791185
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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 |
Pediatrics
|
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 小児免疫 / アレルギー / 膠原病学 / TGF-β / Smadシグナル / 免疫寛容 / T細胞 / 粘膜免疫 / 制御性T細胞 / Th17細胞 / 自己免疫疾患 |
|---|
| Research Abstract |
Transforming growth factor-beta (TGF-β) plays a pivotal role in immunoregulation, yet the role of its intracellular signaling molecules, known as the Smads, had not been established. Previously, we demonstrated that both Smad2 and Smad3 redundantly play essential roles in the immunosuppressive function of TGF-β, including the induction of Foxp3, the master regulator of regulatory T cells. We made a reporter assay system with the luciferase gene under the control of the FOXP3 promoter and enhancer containing Smad-binding element. We confirmed that this reporter assay system worked in Jurkat cells, human T cell line. Furthermore, we demonstrated that not only SMAD3 but also SMAD2 can bind to the enhancer region on FOXP3 gene by using the ChIP assay.
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