2017 Fiscal Year Final Research Report
Possible mechanisms of induction of immunotolerance in appocrine-origin skin tumors
Project/Area Number |
16K19703
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Dermatology
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Research Institution | Tohoku University |
Principal Investigator |
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Project Period (FY) |
2016-04-01 – 2018-03-31
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Keywords | 腫瘍随伴性マクロファージ / RANKL / 乳房外パジェット病 / アポクリン腺癌 |
Outline of Final Research Achievements |
During this research period, we investigated the immunomodulatory effects of cancer stromal factors on tumor-associated macrophages (TAMs), especially focused on RANKL. For example, we have published the immunomodulatory effects of RANKL on M2 macrophages using DNA macroarray analysis, suggesting that RANKL increases the characteristic chemokines, which could be related with immunosuppressive immune cells such as regulatory T cells. We have published these results on Experimental Dermaotology at 2016. In addition, we found that not only M2 macrophages, but also Langerhans cells in the lesional skin of Extramammary Paget’s disease expresses RANK, leading to produce CCL17 by the stimulation of soluble RANKL. We have published these results on Brit J Dermatol at 2017. In aggregate, we have published 11 research papers, all of which possesses impact factor, during our research period.
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Free Research Field |
皮膚科
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