| Project/Area Number |
23390315
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | National Research Institute for Child Health and Development |
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Principal Investigator |
LI Xiao-Kang 独立行政法人国立成育医療研究センター, 移植免疫研究室, 室長 (60321890)
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| Co-Investigator(Kenkyū-buntansha) |
KIMURA Hiromitsu 国立成育医療研究センター, 共同研究管理室, 室長 (80115477)
TAKAHARA Shiro 大阪大学, 先端移植基盤医療学, 教授 (70179547)
OKUMI Masayoshi 大阪大学, 泌尿器学, 助教 (60512978)
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| Project Period (FY) |
2011-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥19,240,000 (Direct Cost: ¥14,800,000、Indirect Cost: ¥4,440,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2013: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2012: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2011: ¥10,270,000 (Direct Cost: ¥7,900,000、Indirect Cost: ¥2,370,000)
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| Keywords | 移植・再生医療 / 幹細胞 / 細胞・組織 |
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| Outline of Final Research Achievements |
During the study period, 1st, we established a method on differentiation DC from murine iPS cells for immune cell therapy. Also, we attempted to generate and characterize DCregs, revealed immune responsiveness regulation effects both in vitro and in vivo, and the ability to generate regulatory T-cells in vitro; 2nd, using mouse tolerant liver transplantation model, we confirmed the presence of MDSC in the grafts, significantly suppressed the T cells proliferation; 3rd, we developed a novel siRNA delivery system, specifically silencing CD40 genes, revealed the effect of the transplanted heart survival prolongation by suppressing the activation of the CD40/CD154 pathway and increased the DCreg cells; Last, we demonstrated that 5-ALA/SFC could inhibited T cell proliferation in response to alloantigens and increased number of regulatory DC and T cells, resulting in permanent cardiac allograft acceptance in mice. These findings highlight the important roles of HO-1 in inducing tolerance.
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