| Project/Area Number |
16591380
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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 |
Digestive surgery
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| Research Institution | University of Tsukuba |
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Principal Investigator |
TAHARA Satoko University of Tsukuba, Graduate School of Comprehensive human sciences, Department of Immunology, Lecturer, 大学院・人間総合科学研究科, 助手 (20360589)
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| Co-Investigator(Kenkyū-buntansha) |
SHIBUYA Kazuko University of Tsukuba, Graduate School of Comprehensive human sciences, Department of Immunology, Assistant Professor, 大学院・人間総合科学研究科, 助教授 (00302406)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2004: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | DNAM-1 / CD226 / CD155 / CD112 / tumor rejection / CD8+T cell / NK cell / memory CTL / DNAM-1(CD226) |
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| Research Abstract |
The poliovirus receptor CD155 and its family member CD112 (nectin-2) are the ligands for the activating cell surface receptor DNAM-1 on CD8+ T cells and NK cells. Here, we demonstrated that, while the RMA tumor grew in syngeneic mice, DNAM-1 ligands-transduced RMA was rejected, in which CD8+ T cells and NK cells played an essential role. Importantly, CD8+ memory cytotoxic T cells to parental RMA were generated in these mice. We found that DNAM-1 was also expressed on CD8α+, rather than CD8α-, dendritic cells. Cross-linking DNAM-1 induced maturation of CD8α+ dendritic cells. Antigen presentation by these stimulated dendritic cells drived Th1 cells. Moreover, the rejection of DNAM-1 ligands-transduced RMA was canceled in CD4+ T cell-depleted and MHC class II deficient mice. Taken together, these results suggest that DNAM-1 ligands stimulate innate immunity by CD8α+ dendritic cells as well as NK cells, which efficiently prime cell-mediated tumor specific immunity.
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