| Project/Area Number |
23791079
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Hematology
|
|---|
| Research Institution | Osaka City University (2012)
Kyoto University (2011) |
|---|
Principal Investigator |
|
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| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
|
|---|
| Keywords | PD-1 / 白血病 / 免疫不全 / leukemia / immunosuppression / osteopontin / immunosenescence |
|---|
| Research Abstract |
When normal young B6 mice were transplanted with leukemia cell lines, PD-1+ CD4+ T cells, which are hardly seen in young mice, were rapidly and robustly increased, and the response of CD4+ T cells to anti -CD3 mAb was profoundly depressed. PD-1+ CD4+ T cells were preferentially detected in the lymphoid tissues with leukemia involvement, suggesting that these T cells constituted a significant host component in leukemic tissues. They exhibited a genetic signature distinct from regular CD4+ T cells including the high expression of C/EBPα, which is normally expressed in myeloid lineage cells. Using TCR transgenic mice as recipients of leukemia, we confirmed that the PD-1+ CD4+ T cells were derived from memory phenotype, but not naive, population.
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