| Project/Area Number |
18K08943
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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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| Review Section |
Basic Section 56010:Neurosurgery-related
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| Research Institution | Kobe University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
篠山 隆司 神戸大学, 医学部附属病院, 教授 (10379399)
田中 一寛 神戸大学, 医学研究科, 講師 (70467661)
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| Project Period (FY) |
2018-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 腫瘍関連マクロファージ / 膠芽腫 / SIRPa / CD47 / 髄液サイトカイン / グリオーマ / 免疫チェックポイント / マクロファージ |
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| Outline of Final Research Achievements |
The infiltration of tumor-associated macrophages (TAM) in glioblastoma was very high. In addition, the expression level of SIRPa was almost the same in low grade glioma as compared with normal brain, and the expression level was decreased in glioblastoma. Also, the expression of CD47 was decreased in glioblastoma. On the other hand, in macrophages, the expression of SIRPa was decreased, but the expression of CD47 was seen. SIRPa antibody was administered to glioblastoma cells, but no significant antitumor effect was obtained. In glioblastoma with weak SIRPa expression, anti-SIRPs antibody alone is likely to be insufficient, and other antibodies, specifically co-antibodies such as PD1 antibody or WT1 antibody, may be required.
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| Academic Significance and Societal Importance of the Research Achievements |
膠芽腫の腫瘍内には多数のM2マクロファージが浸潤しており、独自の免疫環境を構築していることが明らかとなった。一方、膠芽腫の細胞のSIRPaの発現、CD47の発現は正常脳に比較して弱いことが判明した。マクロファージ、膠芽腫細胞のSIRPa-CD47の免疫チェックポイント阻害をSIRPa抗体のみでブロックするだけでは十分な抗腫瘍効果を得ることが出来ない可能性が高く、今後新たな方法を模索する必要がある。
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