2013 Fiscal Year Final Research Report
Investigation on the mechanisms of skin residual deneritic cells in the development psoriasis vulgaris.
| Project/Area Number |
24791189
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Dermatology
|
|---|
| Research Institution | University of Occupational and Environmental Health, Japan |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| 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 |
|---|
| 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.
|
