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首页> 外文期刊>Investigative ophthalmology & visual science >Increased Toll-like receptor-2 expression on nonclassic CD16 + monocytes from patients with inflammatory stage of Eales' disease
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Increased Toll-like receptor-2 expression on nonclassic CD16 + monocytes from patients with inflammatory stage of Eales' disease

机译：Eales病炎症期患者非经典CD16 +单核细胞上Toll样受体2表达增加

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PURPOSE. To identify the distribution, differential Toll-like receptor (TLR) expression, and functional contribution of monocyte subpopulations in the inflammatory stage of Eales' disease (ED). METHODS. Peripheral blood mononuclear cells were isolated from nine patients during the inflammatory stage of ED and nine age- and sex-matched healthy controls. The expression of CD14, CD16, TLR-2, and TLR-4 on monocytes was measured by flow cytometry. The CD14+, CD16-, and CD16+ monocyte populations were sorted on the basis of magnetic-activated cell-sorting methodology, and levels of cytokines were measured by ELISA. RESULTS. In ED patients, the number of circulating monocytes was significantly expanded compared with that in controls (P = 0.01), with a marked increase in the nonclassic CD16+ subset, which showed an activated phenotype in patients that correlated with levels of serum proinflammatory cytokines and clinical progression. A higher expression of cell surface TLR-2 (P = 0.02), but not TLR-4, was found in monocytes of patients with ED. Furthermore, TLR-2 was expressed at higher levels on CD16+ monocytes than on CD16- monocytes in patients, whereas no significant variation was found in TLR-4 expression on different monocyte subsets. Peptidoglycan-induced TNF-α expression correlated with TLR-2 expression in monocytes isolated from controls (r = 0.85, P = 0.0061), but not in monocytes isolated from ED patients (r = 0.553, P = 0.1328). CONCLUSIONS. These results indicate that in the pathogenesis of ED, TLR activation and increased numbers of nonclassic CD16+ monocytes are crucial regulators, along with the secretion of proinflammatory cytokines that perpetuate the inflammatory process in the retina.
机译：目的。为了确定分布，Toll样受体（TLR）的差异表达以及Eales病（ED）炎症阶段单核细胞亚群的功能性贡献。方法。在ED的炎症期和9个年龄和性别匹配的健康对照组中，从9例患者中分离出外周血单个核细胞。通过流式细胞术测量CD14，CD16，TLR-2和TLR-4在单核细胞上的表达。根据磁激活细胞分选方法对CD14 +，CD16-和CD16 +单核细胞群进行分选，并通过ELISA测定细胞因子的水平。结果。在ED患者中，与对照组相比，循环单核细胞的数量显着增加（P = 0.01），非经典CD16 +亚群的显着增加，这表明患者的激活表型与血清促炎细胞因子水平和临床相关进展。 ED患者单核细胞中细胞表面TLR-2的表达较高（P = 0.02），而TLR-4没有。此外，患者中CD16 +单核细胞上TLR-2的表达高于CD16-单核细胞，而在不同单核细胞亚群上TLR-4的表达未见明显变化。肽聚糖诱导的TNF-α表达与从对照中分离出的单核细胞中的TLR-2表达相关（r = 0.85，P = 0.0061），但与从ED患者中分离出的单核细胞中却不相关（r = 0.553，P = 0.1328）。结论。这些结果表明，在ED的发病机制中，TLR激活和非经典CD16 +单核细胞数量的增加是至关重要的调节剂，而促炎细胞因子的分泌则使视网膜的炎症过程得以延续。

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