2016 Fiscal Year Final Research Report
The effects of NKT cell-mediated immunotherapy by IDO inhibitor in mouse lung metastasis model
| Project/Area Number |
26860376
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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 |
Laboratory medicine
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| Research Institution | Fujita Health University (2016)
Suzuka University of Medical Science (2014-2015) |
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Principal Investigator |
Hoshi Masato 藤田保健衛生大学, 医療科学部, 講師 (40633996)
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| Research Collaborator |
SEISHIMA Mitsuru
SAITO Kuniaki
ITO Hiroyasu
HARA Akira
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | インドールアミン酸素添加酵素1 / インドールアミン酸素添加酵素2 / トリプトファン代謝産物 / B16F10細胞 / 抗腫瘍効果 / 細胞免疫療法 |
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| Outline of Final Research Achievements |
The role of indoleamine 2,3-dioxygenase (Ido) in the L-tryptophan (Trp)-kynurenine (Kyn) pathway after lung metastasis model by injecting B16F10 cells was investigated. We used α-GalCer administrated mice of wild type (WT), IDO1 KO, IDO2 KO, and mice treated with 1-methyl-D or L-tryptophan (D or L-1MT), an inhibitor of Ido1 or Ido2 respectively, to study the importance of Trp-Kyn pathway metabolites.
The levels of Ido1 and Ido2 mRNA and protein expression in the lung from WT mice were significantly higher than those from non-injected WT mice. The anti-tumor effect in the lung from IDO1 KO mice or L-1MT treated mice was markedly improved compared to that in WT mice, IDO2 KO mice, and D-1MT treated mice. Moreover, the levels of Trp metabolites in lung from IDO1 KO mice or L-1MT treated mice was significantly decreased compared to that in lung from WT mice, IDO2 KO mice, and D-1MT treated mice.
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| Free Research Field |
病態検査学
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