2016 Fiscal Year Final Research Report
Elucidation of pathogenic mechanism of vitiligo using mice with Th17-type response.
Project/Area Number |
15K15418
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Dermatology
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Research Institution | Osaka University |
Principal Investigator |
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Project Period (FY) |
2015-04-01 – 2017-03-31
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Keywords | 免疫学 / ストレス / 生体分子 |
Outline of Final Research Achievements |
We had reported that significant role of Th17 cells in the development of vitiligo. On the other hand, we found that cellular misfolded proteins/ MHC complex resulted in development of autoimmune diseases. Therefore, we considered that these mechanisms might be involved in vitiligo development. Recently, rhododendrol revealed to induce leukoderma like vitiligo. We thought pathogenesis of rhododendrol-induced vitiligo might have implications for understanding vitiligo. We found that melanocytes were damaged with rhododendrol in the presence of ultraviolet light and an inflammatory cytokine. These effects depended on NF-kB activity. As for establishment of model mice with vitiligo, we cloned several melanocyte antigens of both mice and human, introduced into the expression vector, and confirmed protein expression. We analyzed functions of MHC/melanocyte antigens. We would like to make mice model using the established constructs and the knowledges provided in this study.
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Free Research Field |
皮膚科
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