| Project/Area Number | 13670588 |
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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 | Tohoku University |
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Principal Investigator |
SAIJO Yasuo Tohoku University Graduate School of Medicine, Department of Molecular Medicine and Gene Transfer Research, Associate Professor, 大学院・医学系研究科, 助教授 (10270828)
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| Co-Investigator(Kenkyū-buntansha) |
TOKUE Yutaka Tohoku University School of Medicine, Research Associate, 医学部附属病院, 助手 (80292275)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed(Fiscal Year 2002)
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| Budget Amount *help |
¥3,600,000 (Direct Cost : ¥3,600,000)
Fiscal Year 2002 : ¥1,400,000 (Direct Cost : ¥1,400,000)
Fiscal Year 2001 : ¥2,200,000 (Direct Cost : ¥2,200,000)
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| Keywords | lung cancer / gene thransfer / NKG2D / RAE-1 / Fractalkine / RAE-1 / gene therapy / immunotherapy / C26 |
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| Research Abstract |
NKG2D and its ligand, play a crucial role for innate immunity against to tumor. We developed adenoviral vector coding murine NKG2D ligand RAE-1 (Ad.CMV.RAE-1). When mouse colon cancer cells C26 were infected with Ad.CMV.RAE-1, these cells developed slightly slower than control C26 cells. Because RAE-1 showed very limited effects, we also constructed adenoviral vector expressing CX3C chemokine fractalkine (Ad.CMV.FKN). Intratumoral injection of Ad.CMV.FKN strongly suppressed C26 tumor by 65 % and B16 tumor by 82 %. Immunohistochemistry of tumor treated by Ad.CMV.FKN revealed abundant infiltration of NK cells, CD4 T cells, and CD8 T cells. Vaccinations with Ad.CMV.FKN treated B16 cells inhibited tumor growth of wild type B16. These results indicated that CX3C chemokine induced strong anti-tumor immune responses by recruiting NK cells and T lymphocytes.
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