| Project/Area Number |
15K08523
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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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| Research Field |
Immunology
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| Research Institution | Chiba University |
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Principal Investigator |
YAGI Ryoji 千葉大学, 大学院医学研究院, 特任准教授 (20392152)
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| Research Collaborator |
Sarkar Murshed 千葉大学, 医学薬学府・先端医学薬学専攻博士課程教育リーディングプログラム「免疫システム調節治療学推進リーダー養成プログラム」
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | Th9 / IL-9 / cytokine / CD4T cells / transcription factor / サイトカイン / ヘルパーT細胞 / 転写因子 / Th9細胞 / Th2細胞 / 炎症 |
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| Outline of Final Research Achievements |
Naive CD4 T cells can differentiate into several T helper (Th) cell subsets, Th1, Th2, Th17, regulatory T cells and follicular T cells. Recently Th9 cells have been added into Th cell subsets. Th9 cells are known to induce proliferation of mast cells and secretion of mucus from goblet cells and also to be involved in allergic diseases. IL-4 and TGFβ are required for Th9 cell differentiation from naive CD4 T cells in vitro. However, the molecular mechanism of Th9 cell differentiation and the function of Th9 cells in vivo are not understood yet. To understand the mechanism, we focused on a responsible gene which we found previously, we generated the gene conditional KO mice. Furthermore we established an in vivo model to assess a role of the gene on Th9 cell differentiation.
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