| Project/Area Number |
25461186
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
Suda Takafumi 浜松医科大学, 医学部, 教授 (30291397)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 気管支喘息 / ワクチン療法 / ナノ粒子 / 樹状細胞 / 細胞障害性T細胞 / クロスプレゼンテーション |
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| Outline of Final Research Achievements |
In this study, nanoparticle, which consists of polylactic coglycolic acid (PLGA), was used to induce allergen specific cytotoxic T-lymphocytes (CTL). PLGA facilitates the induction of CTL via cross-presentation machinery in antigen-presenting cells (APC), and these CTL can kill dendritic cell (DC) that plays a role in bronchial asthma.
We found PLGA efficiently induced ovalbumin (OVA)-specific CTL via antigen-presenting cells in vitro. Next, PLGA/OVA was intranasally administered to OVA-induced asthma model mice. PLGA/OVA reduced eosinophil number in bronchoalveolar lavage compared to that after treatment with OVA alone. However, PLGA/OVA could not significantly reduce eosinophil number or induce allergen-specific CTL compared to those of untreated mice. There is a possibility that more manipulation of PLGA/OVA is necessary to improve the delivery and phagocytosis of allergen in APC and to facilitate cross-presentation in vivo.
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