2013 Fiscal Year Final Research Report
A study of RIG-I family dependent ocular surface inflammation
Project/Area Number |
23659817
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Ophthalmology
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Research Institution | Kyoto Prefectural University of Medicine |
Principal Investigator |
KINOSHITA SHIGERU 京都府立医科大学, 医学(系)研究科(研究院), 教授 (30116024)
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Co-Investigator(Kenkyū-buntansha) |
UETA Mayumi 同志社大学, 生命医科学部, 准教授 (60398386)
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Project Period (FY) |
2011 – 2013
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Keywords | 眼免疫学 |
Research Abstract |
Ocular surface epithelium expressed TLR3 and its ligand, polyI:C, stimulation induced the secretion of inflammatory cytokines and type I IFN. It was recently reported that RIG-I and MDA5 also recognize viral dsRNA mimicking polyI:C. In this study, we investigated whether RIG-I and/or MDA5 contribute to polyI:C-inducible responses in conjunctival epithelium. Human conjunctival epithelial cells also expressed RIG-I, MDA-5 and TLR3 mRNA and protein. The expression of RIG-I and MDA-5, but not of TLR3, was markedly up-regulated upon polyI:C stimulation. We also examined the function of IPS-1 and TLR3 in conjunctival epithelium using IPS-1 KO and TLR3 KO mice. Cxcl10, Mx1, Ifi44, Ifi203, Iigp2 and Rtp4 were dominantly regulated by IPS-1, Ccl5 by TLR3, and Rsad2, Mx2 and Cmpk2 were regulated by TLR3 and IPS-1. Our results showed that conjunctival epithelial cells express RIG-I and MDA5,which contributes to polyI:C-inducible cytokine production in conjunctival epithelial cells.
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Research Products
(25 results)
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[Journal Article] Epistatic interaction between Toll-like receptor 3 (TLR3) and prostaglandin E receptor 3 (PTGER3) genes2012
Author(s)
Ueta M, Tamiya G, Tokunaga K, Sotozono C, Ueki M, Sawai H, Inatomi T, Matsuoka T, Akira S, Narumiya S, Tashiro K, Kinoshita S
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Journal Title
J Allergy Clin Immunol
Volume: 129(5)
Pages: 1413-1416.e11
Peer Reviewed
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