Induction of IL-17-producing T cells by VEGF-A as starting molecule: Paradigm shift of psoriasis pathogenesis.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25293243
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Dermatology
• Research Institution: Hamamatsu University School of Medicine
• Principal Investigator: Tokura Yoshiki 浜松医科大学, 医学部, 教授 (00172156)
• Co-Investigator(Kenkyū-buntansha): Hirakawa Satoshi 浜松医科大学, 医学部, 准教授 (50419511)
• Co-Investigator(Renkei-kenkyūsha): Yoshimoto Takayuki 東京医科大学, 医学部, 教授 (80202406) ; Itaka Keiji 東京大学, 医学(系)研究科(研究院), 特任准教授 (60292926)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 免疫学 / 発現制御 / 細胞・組織 / シグナル伝達

Outline of Final Research Achievements

In VEGF-A-K5 transgenic mice, a mouse model of psoriasis, we confirmed that the major IL-17A-producing cells were γδT cells, but not CD4+ T cells, in mice. Plasmacytoid dendritic cells (pDC) were involved in the mechanism underlying IL-17A-producing γδT cells, which stimulate keratinocytes to produce VEGF-A. We found that VEGF-A is a strong chemotactic factor whose activity is comparable to that of chemerin, suggesting that VEGF-A is not only a downstream enhancer but also upstream activator in the psoriasis pathogenesis. We also demonstrated that vitamin D3 depresses the interferon-α production and the chemerin-directed chemotaxis in pDC.

Free Research Field

皮膚科学