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CXC 趋化因子配体 10-CXC 趋化因子受体 3 轴与 CC 趋化因子配体 17-CC 趋化因子受体 4 轴在口腔扁平苔藓发病机制中的相互作用。

Cross-talk between CXC chemokine ligand 10-CXC chemokine receptor 3 axis and CC chemokine ligand 17-CC chemokine receptor 4 axis in the pathogenesis of oral lichen planus.

机构信息

Dept. of Oral Mucosal Diseases, The Affiliated Stomatological Hospital of Nanjing Medical University, Jiangsu Province Key Laboratory of Oral Diseases, Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing 210029, China.

出版信息

Hua Xi Kou Qiang Yi Xue Za Zhi. 2021 Aug 1;39(4):405-412. doi: 10.7518/hxkq.2021.04.005.

Abstract

OBJECTIVES

This study aimed to determine whether a correlation existed between CXC chemokine ligand 10 (CXCL10)-CXC chemokine receptor 3 (CXCR3) and CC chemokine ligand 17 (CCL17)-CC chemokine receptor 4 (CCR4) in the pathogenesis of oral lichen planus (OLP).

METHODS

Peripheral blood of OLP patients (non-erosive and erosive groups) and healthy controls were collected, and T cells were isolated and purified. T cells were co-cultured with three groups: blank, anti-CXCR3, and anti-CCR4. CXCR3 and CCR4 expression were detected by flow cytometry, and CXCL10 and CCL17 were detected by enzyme-linked immunosorbent assay, respectively.

RESULTS

The purities of T cells were all >95% in the three groups (>0.05). Receptor expression showed that CXCR3 and CCR4 in the anti-CXCR3 group was downregulated in OLP compared with the blank group (>0.05). The level of CCR4 in the anti-CCR4 group was significantly downregulated (<0.05), and CXCR3 was upregulated (>0.05). Ligand analysis results showed that CXCL10 in the anti-CXCR3 group was significantly downregulated in OLP compared with the blank group (<0.05), and CCL17 was also downregulated (>0.05). CCL17 in the anti-CCR4 group was significantly downregulated (<0.05), and CXCL10 was upregulated (>0.05). The trend of receptors and ligands in controls was consistent with OLP, but no significant difference existed between the antagonistic and the blank groups (>0.05).

CONCLUSIONS

Two axes interact with each other in the pathogenesis of OLP and may play different roles in its occurrence and development.

摘要

目的

本研究旨在探讨细胞趋化因子配体 10(CXCL10)-细胞趋化因子受体 3(CXCR3)与 C 型趋化因子配体 17(CCL17)-C 型趋化因子受体 4(CCR4)在口腔扁平苔藓(OLP)发病机制中的相关性。

方法

收集 OLP 患者(非糜烂型和糜烂型)和健康对照者外周血,分离和纯化 T 细胞。将 T 细胞与三组细胞共培养:空白组、抗-CXCR3 组和抗-CCR4 组。采用流式细胞术检测 CXCR3 和 CCR4 的表达,酶联免疫吸附试验检测 CXCL10 和 CCL17 的表达。

结果

三组 T 细胞纯度均>95%(>0.05)。受体表达显示,与空白组相比,抗-CXCR3 组 OLP 中 CXCR3 和 CCR4 的表达下调(>0.05)。抗-CCR4 组 CCR4 水平明显下调(<0.05),而 CXCR3 水平上调(>0.05)。配体分析结果显示,与空白组相比,抗-CXCR3 组 OLP 中 CXCL10 明显下调(<0.05),CCL17 也下调(>0.05)。抗-CCR4 组 CCL17 明显下调(<0.05),而 CXCL10 上调(>0.05)。对照组的受体和配体趋势与 OLP 一致,但拮抗组与空白组之间无显著性差异(>0.05)。

结论

两条轴在 OLP 的发病机制中相互作用,可能在其发生和发展中发挥不同的作用。

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