Elucidation of regulation mechanisms for inflammation though TLR3-EP3 interaction

2015 Fiscal Year Final Research Report

• Project/Area Number: 25462762
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Ophthalmology
• Research Institution: Kyoto Prefectural University of Medicine (2015); Doshisha University (2013-2014)
• Principal Investigator: UETA MAYUMI 京都府立医科大学, 医学(系)研究科(研究院), 准教授 (60398386)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 自然免疫 / 眼表面上皮 / TLR3 / EP3

Outline of Final Research Achievements

We elucidated the regulation mechanisms via the innate immune system in the ocular surface epithelial cells, in particular, we focused the regulation mechanisms through the TLR3-EP3 interaction. We clarified that TLR3 stimulation could induce various gene expression in ocular surface epithelial cells, and the genes expression could be reduced by EP3 stimulation. In addition, we found that the upregulation of genes which were found in EP3 KO mice were canceled in TLR3/ EP3 double KO mice, suggesting that EP3 could suppress the TLR3 inducible gene expression.

Free Research Field

眼表面の粘膜免疫ならびに自然免疫