The analysis of the immune-inhibitory molecules in refractory inflammatory oral mucous disease and the basic research for development of new therapy.
| Project/Area Number |
20592321
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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 |
Surgical dentistry
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
TSUSHIMA Fumihiko Tokyo Medical and Dental University, 歯学部附属病院, 医員 (90456210)
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| Co-Investigator(Kenkyū-buntansha) |
AZUMA Miyuki 東京医科歯科大学, 大学院・医歯学総合研究科, 教授 (90255654)
SAKURAI Jinkyo 東京医科歯科大学, 大学院・医歯学総合研究科, 講師 (30361710)
ITO Daisuke 東京医科歯科大学, 大学院・医歯学総合研究科, 非常勤講師 (40286844)
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| Project Period (FY) |
2008 – 2011
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 口腔外科一般 / 口腔粘膜疾患 / 口腔癌 / 免疫抑制分子 / 上皮角化細胞 / 免疫療法 |
|---|
| Research Abstract |
In this study, to investigate the function of B7-H1 on KC, we generated transgenic (tg) mice overexpressing B7-H1 under the control of human keratin 14 (K14) promoter (B7-H1 tg). In DNFB hapten-induced contact hypersensitivity model, it suggests that B7-H1 on KC may directly downregulate the effector function of CD8 T cells at skin inflammatory site. Furthermore, it indicates that B7-H1 on KC accelerates carcinogenesis by promoting epithelial-mesenchymal transition via down-regulation of E-cadherin on KC in a methylcholantrene(MCA)-induced model of squamous cell carcinoma(SCC).
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Report
(4 results)
Research Products
(23 results)
