| Project/Area Number |
25830124
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor therapeutics
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
SUZUKI TORU 兵庫医科大学, 医学部, 講師 (00441296)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | γδ T細胞 / PD-1 / 4-1BB / 副刺激 / PD1 |
|---|
| Outline of Final Research Achievements |
Anti-4-1BB antibody and anti-PD-L1 antibody combined with TCR stimulation significantly up-regulated CD69 expression and inhibited activation induced cell death of γδ T cells. Although anti-4-1BB and anti-PD-L1 antibody enhanced secretion of IFNγ and perforin, granzyme compared with TCR stimulation alone, we didn’t observed significant increase. Finally, antitumor effects of γδ T cells against human bladder cancer cells didn’t increase upon co-stimulation with both antibodies. That is the reason why the ratio of 4-1BB and PD-1 positive γδ T cells decreased after 10 days of culture. Therefore, it is needed to use only 4-1BB and PD-1 positive γδ T cells for new adoptive γδ T cell therapy regulated through co-stimulatory and co-inhibitory receptor.
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