| Project/Area Number |
21590415
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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 |
Experimental pathology
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| Research Institution | Gifu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
GOTOH Naoe 岐阜大学, 大学院・医学系研究科, 講師 (80444280)
KITOH Yusuke 岐阜大学, 大学院・医学系研究科, 助教 (80444305)
齊尾 征直 琉球大学, 医学部附属病院, 准教授 (40242721)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | TIM / M1マクロファージ / M2マクロファージ / 骨髄由来サプレッサー細胞(MDSC) / 抗原呈示樹状細胞 / GM-CSF / M-CSF siRNA / 可塑性 / 骨髄細胞由来サプレッサー細胞(MDSC) / tumor associated macrophage / M1 macrophage / M2 macrophage / siRNA / M-CSF receptor / 日ハンガリー科学技術協力 / myeloid-derived suppressor cell / mRNA / Hungary |
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| Research Abstract |
The marker profile, production of cytokine and chemokine, and antigen-presenting capability were studied to clarify the origin of tumor-infiltrating macrophages(TIM). Our results clearly showed that TIM was the hetrogeneous cell population having both capabilities of tumor-suppressing(M1) macrophage and tumor-promoting(M2) macrophages. On the other hand, the treatment of TIM with GM-CSF and siRNA for M-CSF induced the intra-cellular signal transducing molecules such as STAT-1, STAT-5, and STAT-6 of which are necessary for maturation toward antigen-presenting dendritic cells, nevertheless the maker-profiles of treated TIM did not change significantly. However both of the GM-CSF and siRNA for M-CSFR treated and non-treated TIM revealed similar antigen presenting capabilities in the system using OVA-specific TCR transgenic mice. Altogether it was clarified that the phenotype of TIM was reflecting the invading tumor microenvironment, and not certain cell type such as myeloid-derived suppressor cells, but was the cell that still keeped plasticity and could be changed by surrounding microenvironment.
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