| Project/Area Number |
22790925
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
膠原病・アレルギー・感染症内科学
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| Research Institution | Chiba University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ヘルパーT細胞分化 / Ikarosファミリー分子 / Helios / 制御性T細胞 |
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| Research Abstract |
We have recently shown that Helios, an Ikaros family of transcription factor, is highly expressed in CCR6+CD4+CD45RO+ T cells as compared with that in CCR6-CD4+CD45RO+ T cells. However, the role of Helios in T cell differentiation remains largely unknown. Therefore, in this study, we examined the role of Helios in the differentiation of murine CD4+ T cells. We first examined the effect of various cytokines on the expression of Helios in TCR-stimulated murine splenic CD4+ T cells and found that TGF-β induced Helios expression in CD4+ T cells. In contrast, IL-6 inhibited Helios expression in a Stat3-dependent manner. Retroviral-mediated expression of Foxp3 in the absence of TGF-β did not induce Helios expression in CD4+ T cells. On the other hand, enforced expression of Helios up-regulated activation markers of regulatory T cells (Tregs) such as CD103 and GITR in Foxp3+ Tregs. These results suggest that TGF-β may enhance Treg function through the induction of Helios expression in a Foxp3-independent fashion.
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