2016 Fiscal Year Final Research Report
Molecular mechanism of skin inflammation induced by desmoglein 3-specific T cells
| Project/Area Number |
26293258
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Keio University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
佐々木 貴史 慶應義塾大学, 医学部, 講師 (70306843)
天谷 雅行 慶應義塾大学, 医学部, 教授 (90212563)
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| Research Collaborator |
O'Shea John National Institutes of Health, National Institute of Musculoskeletal and Skin Diseases
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | Interface dermatitis / Desmoglein / T cell |
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| Outline of Final Research Achievements |
Interface dermatitis is a pathological feature which is commonly observed in a variety of skin diseases including lichen plans, severe drug adverse reaction, graft-versus-host disease, paraneoplastic pemphigus and so on. The molecular mechanism that leads to interface dermatitis has not been understood. In this project, we took advantage of genetically engineered mice and discovered that T-bet and Stat1, crucial transcriptional factors in T cell differentiation, are keys in development of interface dermatitis. On the other hand, we also sought to establish a novel concept in the field of Immunology in this project. Through investigating genes which are specifically induced by interleukin (IL)-27, we found that cholesterol metabolizing enzyme is induced by IL-27 and the function contributes to immune regulation. Our results are promisingly expected to be useful to invent a new treatment for skin inflammatory diseases in the future.
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| Free Research Field |
皮膚免疫
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