| Project/Area Number |
24791189
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Dermatology
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| Research Institution | University of Occupational and Environmental Health, Japan |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 尋常性乾癬 / ランゲルハンス細胞 / ガンマデルタＴ細胞 / Ｔｈ１７ / IL-23 / IL-17 / インターロイキン２３ / ガンマデルタT細胞 / インターロイキン１７ / IL-12/23p40 / gamma-delta T細胞 |
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| Research Abstract |
Psoriasis is a common chronic inflammatory skin disease that involves dysregulated interplay between immune cells and keratinocytes. Langerhans cells (LCs) are a subset of dendritic cells that reside in the epidermis and regulate immune responses. In this study, we focused on Th17-related factors and assessed the role of LCs and gamma-delta T cells in the development of psoriasis using a mouse psoriasis model triggered by topical application of imiquimod (IMQ). Langerhans cell depletion by means of diphtheria toxin (DT) in Langerin DT receptor-knocked-in mice suppressed hyperkeratosis, parakeratosis and ear swelling in the IMQ-treated regions. In addition, LC-depleted mice showed decreased levels of Th17-related cytokines in IMQ-treated skin lesions. These results suggest that LCs are required for the development of psoriasis-like lesions induced by IMQ in mice.
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