Triggering of TLR3 by polyI:C in human corneal epithelial cells to induce inflammatory cytokines
Triggering of TLR3 by polyI:C in human corneal epithelial cells to induce inflammatory cytokines
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DOI：
10.1016/j.bbrc.2005.02.196
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发表时间：
2005-05-27
影响因子：
3.1
通讯作者：
Kinoshita, S
中科院分区：
文献类型：
--
作者：
Ueta, M;Hamuro, J;Kinoshita, S
眼表上皮细胞作为粘膜免疫系统对抗病原体的一部分，是一线防御的关键。我们研究了polyI:C是否诱导人角膜上皮细胞（HCEC）产生促炎细胞因子和IFN-β，以及Toll样受体（TLR）-3的表达是否被polyI:C放大。 TLR3在HCEC表面表达。 PolyI:C 刺激引起 HCEC 中 IL-6 和 IL-8 的产生和 mRNA 表达升高。虽然 PolyI:C 在 HCEC 中诱导 IFN-β 和 TLR3 基因表达（远强于人成纤维细胞），但 LPS 刺激则不然。同样，在 HCEC 中，polyI:C（而非 LPS）诱导 I kappa B α 和 MAIL（I kappa B 家族成员）的基因表达。 HCEC 的先天免疫反应与免疫活性细胞不同，我们认为这表明角膜上皮和眼表微生物之间存在共生关系。 (c) 2005 Elsevier Inc. 保留所有权利。
Epithelial cells of the ocular surface are key in the first-line defense as a part of the mucosal immune system against pathogens. We investigated whether polyI:C induces the production by human corneal epithelial cells (HCEC) of pro-inflammatory cytokines and IFN-beta, and whether Toll-like receptor (TLR)-3 expression is amplified by polyI:C. TLR3 was expressed on the surface of HCEC. Stimulation with polyI:C elicited the elevated production and mRNA expression of IL-6 and IL-8 in HCEC. While polyI:C induced IFN-beta, far stronger than human fibroblasts, and TLR3 gene expression in HCEC, LPS stimulation did not. Similarly, polyI:C, but not LPS, induced the gene expression of I kappa B alpha and MAIL, members of the I kappa B family, in HCEC. The innate immune response of HCEC is distinct from that of immune-competent cells, and we suggest that this is indicative of the symbiotic relationship between corneal epithelium and microbes inhabiting the ocular surface. (c) 2005 Elsevier Inc. All rights reserved.