| Project/Area Number |
20590894
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Chiba University |
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Principal Investigator |
HIROSE Koichi Chiba University, 医学部附属病院, 助教 (90400887)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Norihiko 千葉大学, 医学部附属病院, 講師 (20375653)
IKEDA Kei 千葉大学, 医学部附属病院, 助教 (10456014)
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| Co-Investigator(Renkei-kenkyūsha) |
NAKAJIMA Hiroshi 千葉大学, 大学院・医学研究院, 教授 (00322024)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | Dectin-1 / IL-10産生性CD4陽性T細胞 / STAT6 / c-Maf / 気管支喘息 / T-bet / ICOS-ICOSL / TGFβ / 真菌 / Dection-1 / β-glucan / IL-10産生性T細胞 / Th17細胞 |
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| Research Abstract |
Recent evidence suggests that signals through not only Toll-like receptors(TLR) but also Dectin-1 contribute to the fine-tuning of acquired immune responses. Here, we examined the effect of Dectin-1 signaling on CD4+ T cell differentiation by using a linear form of pure β-glucan, curdlan, as a ligand. We found that curdlan instructed DCs to induce the development of IL-10-producing CD4+ T cells without the significant production of IFN-γ, IL-4, or IL-17A. We also found that IL-10-producing CD4+ T cells did not express T-bet, GATA3, RORγt, or FoxP3, but expressed c-Maf, which has been shown to activate the transcription of IL-10. Moreover, we found that STAT6 but not T-bet expressed in the CD4+ T cells is essential for the IL-10 producing T cell differentiation induced by curdlan. Taken together, these results suggest that STAT6 as well as c-Maf plays a critical role for the development of IL-10-producing CD4+ T cells in the presence of Dectin-1 activation.
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