| Project/Area Number |
18580323
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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 |
Clinical veterinary science
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| Research Institution | Nippon Veterinary and Life Science University |
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Principal Investigator |
BONKOBARA Makoto Nippon Veterinary and Life Science University, Department of veterinary medicine, Lecturer (50343611)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥300,000)
Fiscal Year 2007: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2006: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | dendritic cells / T-cells / suppression / antigen / co-stimulation |
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| Research Abstract |
I investigated dendritic cell-mediated antigen specific T-cell proliferation and suppression in this year. The reaction was studied on animals in vivo in previous year ; however, the study was not enough to validate specific reaction of T-cells. Therefore, in vitro analysis system was developed this year (Tamura, et. al. Journal of Veterinary Medical Science 2007). Using antigen prepared from malignant melanoma or malignant lymphoma, dendritic cells were pulsed and proliferation of lymphocytes were examined. Although dendritic cells loaded with antigen prepared from malignant melanoma induced proliferation of lymphocytes, dendritic cells loaded with antigen prepared from malignant lymphoma failed proliferation of lymphocytes. Dendritic cells loaded with antigen prepared from malignant melanoma express undetectable levels of DC-HIL, while that loaded with antigen prepared from malignant lymphoma showed high level expression of DC-HIL. The data suggested that DC-HIL is a molecule closely associates suppression of T cell proliferation. From this study, it was considered that DC-HIL control antigen-specific suppression of T cell and its abnormality may disrupt tolerance of T cells to self-tissues.
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