| Project/Area Number |
15H06247
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Tumor therapeutics
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| Research Institution | Gifu University |
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Principal Investigator |
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| Project Period (FY) |
2015-08-28 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 腫瘍免疫 / アリルハイドロカーボン受容体 / キヌレニン / 癌 / 免疫 |
|---|
| Outline of Final Research Achievements |
IDO is an intracellular enzyme proceed the essential amino acid tryptophan metabolism. Accumulation of tryptophan derivatives such as kynurenine blocks antigen-specific T-cell proliferation and induces T-cell death. A recent study indicated that kynurenine was an endogenous ligand of aryl hydrocarbon receptor (AhR). We collected PBMCs from healthy blood donors, and bone marrow samples from multiple myeloma patients at first diagnosis. The cells were activated with anti-CD3 and anti-CD28 Abs. We measured the expression of AhR in activated T-cells using by flow cytometry.Kynurenine produced by IDO, induce inhibitory signal in T-cells through the AhR. Anti-PD-1 and anti-CTLA-4 therapies, which block directly the inhibitory signal in T-cells, have been getting some clinical benefits against such as melanoma and Hodgkin lymphoma. Therefore, the AhR in T cells might be a target for IDO-positive hematological malignancies.
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