2017 Fiscal Year Final Research Report
Investigation of mechanisms for the regulation of CD8 T cell exhaustion by type 2 diabetic drug, metfromin
Project/Area Number |
16K18452
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Tumor therapeutics
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Research Institution | Okayama University |
Principal Investigator |
Eikawa Shingo 岡山大学, 医歯薬学総合研究科, 助教 (40635265)
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Project Period (FY) |
2016-04-01 – 2018-03-31
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Keywords | CD8 T細胞 / 代謝免疫 / メトホルミン / 好気的解糖 / グルコース / アミノ酸 |
Outline of Final Research Achievements |
We previously argued that type 2 diabetic drug, metformin has an anti tumor effect mediated by the modulation of CD8 T cell function. In this study, we investigated further mechanisms of the effect on several mouse tumor implantation model. These results revealed the activation of AMPK in antigen-specific CD8 T cell by metformin is quite important for tumor regression. Metformin-induced AMPK activation led to enhance an aerobic glycolysis of CD8 T cell through cell membrane translocation of amino acid transpoter, LAT1. These data indicated CD8 T cell metabolism has an critical role for anti-tumor effect of metformin.
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Free Research Field |
がん免疫
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