Effects of Interleukin-17(IL-17) and IL-17 receptor on ocular surface inflammation
Project/Area Number |
23792011
|
Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Ophthalmology
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Research Institution | Nihon University |
Principal Investigator |
YAMADA AI 日本大学, 医学部, 助教 (30535191)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
|
Keywords | IL-17レセプター / 眼表面 / 発現制御 / 炎症 / IL-17 / IL-17R / 角膜上皮細胞 / 角膜実質細胞 / Exotoxin A / マウスアルカリ角膜外傷モデル / IL-6 / CCL20 / 前眼部炎症 |
Research Abstract |
The cornea is the transparent window covering the front of the eye. It is a refracting surface, and also serves as a barrier of the eye. If the cornea is deeply injured or robust inflammation occurs, it leaves a scar, which leads to vision loss. Recently, Interleukin17 (IL-17)-producing helper T cell subset Th17 has been discovered. It has reported that IL-17 is a major contributor of autoimmune inflammation such as rheumatoid arthritis. In this research, we focused on the corneal inflammation and the IL-17 receptor expression. We discovered that upon corneal alkali injury or corneal infection, the expression of IL-17 receptor in the cornea is up-regulated.
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Report
(4 results)
Research Products
(6 results)