Project/Area Number |
26860376
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Laboratory medicine
|
Research Institution | Fujita Health University (2016) Suzuka University of Medical Science (2014-2015) |
Principal Investigator |
Hoshi Masato 藤田保健衛生大学, 医療科学部, 講師 (40633996)
|
Research Collaborator |
SEISHIMA Mitsuru
SAITO Kuniaki
ITO Hiroyasu
HARA Akira
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
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 / IDO1 / IDO2 / B16F10 / IDO1 / IDO2 / B16F10 / α-ガラクトシルセラミド / トリプトファン代謝 / 1-MT / IDO / B16細胞 / α-ガラクトシルセラミド / トリプタファン代謝 / 1-metyl-D-tryptophan / 1-metyl-L-tryptophan |
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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