A study of RIG-I family dependent ocular surface inflammation

眼表上皮表达TLR 3及其配体polyI：C，刺激诱导炎性细胞因子和I型IFN的分泌。 最近报道RIG-I和MDA 5也识别模拟polyI：C的病毒dsRNA。在这项研究中，我们调查是否RIG-I和/或MDA 5有助于polyI：C诱导的反应，结膜上皮。人结膜上皮细胞也表达RIG-I、MDA-5和TLR 3 mRNA和蛋白。 RIG-I和MDA-5的表达，而不是TLR 3，在polyI：C刺激后显著上调。我们还使用IPS-1 KO和TLR 3 KO小鼠检测了IPS-1和TLR 3在结膜上皮中的功能。Cxcl 10、Mx 1、Ifi 44、Ifi 203、Iigp 2和Rtp 4主要受IPS-1的调控，Ccl 5主要受TLR 3的调控，Rsad 2、Mx2和Cmpk 2主要受TLR 3和IPS-1的调控。 我们的研究结果表明，结膜上皮细胞表达RIG-I和MDA 5，这有助于在结膜上皮细胞中产生polyI：C诱导的细胞因子。

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.