2013 Fiscal Year Final Research Report

Effects of Interleukin-17(IL-17) and IL-17 receptor on ocular surface inflammation

Research Project

Project/Area Number	23792011
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Ophthalmology
Research Institution	Nihon University
Principal Investigator	YAMADA AI 日本大学, 医学部, 助教 (30535191)
Project Period (FY)	2011 – 2013
Keywords	IL-17レセプター / 眼表面 / 発現制御 / 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.