| Project/Area Number |
17013024
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | University of Toyama (2006-2009)
The University of Tokyo (2005) |
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Principal Investigator |
TAKATSU Kiyoshi University of Toyama, 大学院・医学薬学研究部, 教授 (10107055)
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| Co-Investigator(Kenkyū-buntansha) |
NAGAI Yoshinori 富山大学, 医学薬学研究部, 准教授 (30431761)
KARIYONE Ai 富山大学, 医学薬学研究部, 助教 (50114450)
IKUTANI Masashi 富山大学, 医学薬学研究部, 助教 (40513718)
TAMURA Toshiki ハンセン病研究センター, 室長 (40291306)
HONDA Hiroe 富山県薬事研究所, 主任研究員 (10463134)
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| Project Period (FY) |
2005 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥53,500,000 (Direct Cost: ¥53,500,000)
Fiscal Year 2009: ¥10,700,000 (Direct Cost: ¥10,700,000)
Fiscal Year 2008: ¥10,700,000 (Direct Cost: ¥10,700,000)
Fiscal Year 2007: ¥10,700,000 (Direct Cost: ¥10,700,000)
Fiscal Year 2006: ¥10,700,000 (Direct Cost: ¥10,700,000)
Fiscal Year 2005: ¥10,700,000 (Direct Cost: ¥10,700,000)
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| Keywords | Ag85B / Peptide-25 / Th1 / Th2 / 抗原提示細胞 / クロスプレゼンテーション / 抗腫瘍免疫増強 / IFN-γ / アジュバント活性 / 結核菌 / 癌 / 免疫学 / IFN--γ / アジュバント効果 / CD40-CD40L / 細胞障害活性 / Th1抗原ペプチド / I-A拘束性 / トランスジェニックマウス |
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| Research Abstract |
(1) Using P25 TCR-Tg mice, we demonstrated that direct interaction between TCR and peptide-loaded antigen-presenting cells primarily determines the fate of naive CD4^+ T cells, even in the absence of T-bet expression and costimulatory signals. (2) Coimmunization of mice with P25 and OVA resulted in the enhancement of CD8^+ cytotoxic T cells specific for OVA and growth inhibition of EL-4 thymoma expressing OVA peptide leading to the tumour rejection, indicating that P25 exerts a potent adjuvant activity for antitumour immunity. (3) P25-stimulated P25 CD4^+ T cells augment antigen cross-presentation by APC. IFN-γ and IFN-γ-inducible genes play indispensable roles the Th1-mediated cross-presentation.
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