| Project/Area Number |
23249064
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Hiroshima University |
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Principal Investigator |
OHDAN Hideki 広島大学, 医歯薬保健学研究院, 教授 (10363061)
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| Co-Investigator(Kenkyū-buntansha) |
IDE Kentaro 広島大学, 大学病院, 病院助教 (50511565)
KOBAYASHI Takaaki 名古屋大学, 医学系(医)研究科(研究院), 寄付講座教授 (70314010)
TAHARA Hidetoshi 広島大学, 医歯薬保健学研究院, 教授 (00271065)
SHIMAMOTO Akira 広島大学, 医歯薬保健学研究院, 准教授 (70432713)
TANAKA Yuka 広島大学, 医歯薬保健学研究院, 助教 (90432666)
安井 弥 広島大学, 医歯薬保健学研究院, 教授 (40191118)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥48,230,000 (Direct Cost: ¥37,100,000、Indirect Cost: ¥11,130,000)
Fiscal Year 2013: ¥13,780,000 (Direct Cost: ¥10,600,000、Indirect Cost: ¥3,180,000)
Fiscal Year 2012: ¥14,170,000 (Direct Cost: ¥10,900,000、Indirect Cost: ¥3,270,000)
Fiscal Year 2011: ¥20,280,000 (Direct Cost: ¥15,600,000、Indirect Cost: ¥4,680,000)
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| Keywords | 腫瘍免疫 / 免疫回避 / 分子標的治療 / 糖鎖抗原 |
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| Research Abstract |
We investigated whether inhibition of CD47-SIRPa signaling increases macrophage phagocytic activity against cancer cells by using in vitro and in vivo mouse syngeneic models. CD47 knock down Hepa1-6 cells were significantly more sensitive to macrophage phagocytosis than parental Hepa1-6 cells in both of in vitro and in vivo phagocytosis assays, indicating the pivotal role of CD47-SIRPa interaction in restricting tumor cell killing. Addition of anti-SIRPa mAns markedly enhanced the phagocytic activity of peritoneal cavity macrophage against Hepa1-6 and CMT93 compared with the isotype-matched Ab treatment in both of the in vitro and in vivo phagocytosis assays. Thus, our results suggest that CD47-SIRPa signaling interaction is a therapeutic target for inhibiting the growth of cancer cells.
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