| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Outline of Final Research Achievements |
ATL cells usually express forkhead box P3 (FOXP3). However, the mechanisms of FOXP3 expression remain unclear. Analysis of DNA methylation in ATL showed a part of patients hypomethylated the TSDR. Flowcytometric analysis showed CD3+CD4+TSLC-1+CD7- cells were mainly HTLV-1-infected cells and possess the regulatory T cell (Treg) phenotype, such as FOXP3, CCR4. Loss of CD58 is a common mechanism for tumor immune evasion in lymphoid malignancies. Epigenetic library screening demonstrated that EZH2 inhibitors enhanced CD58 expression. EZH2 inhibitor enhanced interferon-γ production of T and NK cells against lymphoma cells. These results indicated that downregulation of CD58 could be a mechanism for tumor immune escape and provide a molecular basis for immunotherapy.
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