| Project/Area Number |
21590984
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KAGAMU Hiroshi 新潟大学, 医歯学系, 講師 (30418686)
YOSHIZAWA Hirohisa 新潟大学, 医歯学総合病院, 准教授 (50282984)
NAKATA Ko 新潟大学, 医歯学総合病院, 教授 (80207802)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 非閉塞性肺疾患癌 / 肺線維症 / 呼吸器感染症 / その他 / 非特異的肺疾患癌 / 抑制性T細胞 / 化学療法 / MDSC / 腫瘍免疫療法 / 抗腫瘍免疫療法 / 放射線療法 |
|---|
| Research Abstract |
Previously, we found that radio-resistant Treg inhibited the development of antitumor immunity. In the current study, we also found that Treg was increased in cyclophosphamide treated mice. Depletion of Treg with anti-CD25 antibodies after cyclophosphamide treatment significantly augmented antitumor immune responses and eradicated advanced skin-tumors.
CD25 is expressed on both of Treg and activated T cells. Anti-CD25 antibodies potentially deplete antitumor effector T cells. Thus, we have examined whether anti-TGF-b antibodies and anti-CTLA-4 antibodies efficiently deplete Treg in mice treated with cyclophosphamide.
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