2020 Fiscal Year Final Research Report
Generation of novel mouse model for psoriasis focusing on regulatory T cell
| Project/Area Number |
19K17790
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 53050:Dermatology-related
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| Research Institution | Hokkaido University |
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Principal Investigator |
Ujiie Inkin 北海道大学, 大学病院, 医員 (40822705)
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| Project Period (FY) |
2019-04-01 – 2021-03-31
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| Keywords | 乾癬 / Stat6 / T-bet / Foxp3 / イミキモド / サイトカイン / IL-17 |
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| Outline of Final Research Achievements |
Psoriasis vulgaris is a common inflammatory keratotic disease. Th1/Th2/Th17 balance in psoriasis is still largely unknown because the evidence of the Th balance by in vivo studies is limited. We analyzed the experimental psoriasis model induced by topical imiquimod using T-bet (Th1) and Stat6 (Th2) double knockout (DKO) mice and found that the imiquimod-treated ear thickness is thicker in DKO mice than wild type (WT) mice and IL-17-producing CD4+ T cells in the lesional skin are increased in DKO mice compared to those in WT mice, suggesting the positive-correlation between the number of IL-17-producing CD4+T cells and the imiquimod-treated ear thickness.
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| Free Research Field |
皮膚科学
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| Academic Significance and Societal Importance of the Research Achievements |
本研究結果は、IL-17産生CD4+T細胞（Th17）の増加が、イミキモド誘発性乾癬モデルの炎症の増強に関与していることを示唆している。つまり、乾癬におけるTh17細胞の重要性が新規乾癬モデルマウスによって示された。今後はこの系を発展させ、制御性T細胞（Treg）のマスター転写因子であるFoxp3をノックアウトさせたFoxp3, T-bet, Stat6トリプルノックアウトマウスを作成することで乾癬におけるTregの役割を明らかにし、更なる病態解明につなげていきたい。
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