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转化生长因子-β(TGF-β)和白细胞介素-1β(IL-1β)协同作用,可提高人视网膜色素上皮细胞中白细胞介素-6(IL-6)和白细胞介素-8(IL-8)的信使核糖核酸(mRNA)水平以及IL-6的生成量。

TGF-beta and IL-1 beta act in synergy to enhance IL-6 and IL-8 mRNA levels and IL-6 production by human retinal pigment epithelial cells.

作者信息

Kuppner M C, McKillop-Smith S, Forrester J V

机构信息

Department of Ophthalmology, University of Aberdeen, Medical School, UK.

出版信息

Immunology. 1995 Feb;84(2):265-71.

PMID:7751003
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1415109/
Abstract

Cytokines produced by human retinal pigment epithelial (RPE) cells may function as important regulators of intraocular inflammation. We investigated the effect of transforming growth factor-beta (TGF-beta) on interleukin-1 beta (IL-1 beta) induction of IL-6 and IL-8 mRNA levels and protein production by human RPE cells. Both TGF-beta and IL-1 beta alone induce IL-6 mRNA and IL-6 production in human RPE cells and synergize to enhance IL-6 mRNA levels and IL-6 production over a range of TGF-beta (0.1-10 ng/ml) and IL-1 beta concentrations (5-500 U/ml). TGF-beta was also found to enhance IL-1 beta induction of IL-8 mRNA levels at lower IL-1 beta concentrations (50 U/ml) but had no effect at higher IL-1 beta concentrations (500 U/ml). However, TGF-beta had no synergistic effect on IL-1 beta induction of IL-8 secretion. These results suggest that expression of IL-6 and IL-8 in human RPE cells is regulated by different transcriptional and translational mechanisms, and that RPE cells are important regulators of cytokine production within the ocular microenvironment.

摘要

人视网膜色素上皮(RPE)细胞产生的细胞因子可能作为眼内炎症的重要调节因子。我们研究了转化生长因子-β(TGF-β)对白细胞介素-1β(IL-1β)诱导人RPE细胞中白细胞介素-6(IL-6)和白细胞介素-8(IL-8)mRNA水平及蛋白产生的影响。单独的TGF-β和IL-1β均可诱导人RPE细胞中IL-6 mRNA和IL-6的产生,并在一系列TGF-β(0.1 - 10 ng/ml)和IL-1β浓度(5 - 500 U/ml)范围内协同增强IL-6 mRNA水平和IL-6的产生。还发现TGF-β在较低IL-1β浓度(50 U/ml)时可增强IL-1β对IL-8 mRNA水平的诱导作用,但在较高IL-1β浓度(500 U/ml)时无作用。然而,TGF-β对IL-1β诱导的IL-8分泌无协同作用。这些结果表明,人RPE细胞中IL-6和IL-8的表达受不同的转录和翻译机制调控,并且RPE细胞是眼内微环境中细胞因子产生的重要调节因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e751/1415109/b1509c77e205/immunology00072-0099-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e751/1415109/d9e5339456d3/immunology00072-0097-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e751/1415109/10172a8b3cff/immunology00072-0098-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e751/1415109/b1509c77e205/immunology00072-0099-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e751/1415109/d9e5339456d3/immunology00072-0097-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e751/1415109/10172a8b3cff/immunology00072-0098-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e751/1415109/b1509c77e205/immunology00072-0099-a.jpg

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