Overexpression and selectively regulatory roles of IL-23/IL-17 axis in the lesions of oral lichen planus.

Overexpression and selectively regulatory roles of IL-23/IL-17 axis in the lesions of oral lichen planus.
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IL-23/IL-17轴在口腔扁平苔藓病变中的过表达及选择性调节作用

DOI:
10.1155/2014/701094
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发表时间:
2014
影响因子:
4.6
通讯作者:
Chen Q
Chen Q
中科院分区:
医学3区
文献类型:
--
作者:
Lu R;Zeng X;Han Q;Lin M;Long L;Dan H;Zhou G;Chen Q

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白细胞介素-(IL-)23/IL-17轴是一种新发现的促炎症信号通路,与许多慢性炎症和免疫疾病的发病机制有关。在这里,我们调查了IL-23/IL-17轴是否存在于口腔扁平苔藓(OLP),一种影响口腔粘膜的慢性炎症性疾病的病变和功能。应用免疫组化和定量PCR技术,我们发现IL-23和IL-17在OLP病变组织中的表达高于正常口腔粘膜组织。IL-23和IL-17在OLP网状组织中的表达呈正相关。体外研究结果显示,外源性IL-23可增加网状型OLP患者外周血Th17细胞的比例,并增加CD4 + T细胞IL-17的分泌。此外,我们还发现外源性IL-17可显著增强人口腔角质形成细胞中β-防御素-2、-3、CCL-20、IL-8和TNF-α的mRNA表达,但对β-防御素-1、CXCL-9、-10、-11、CCL-5和IL-6的mRNA表达无明显影响。综上所述,我们的研究结果揭示了IL-23/IL-17轴在OLP病变中的过度表达模式和选择性调节作用,表明它可能是OLP病变复杂免疫网络中的关键调节途径。
Interleukin- (IL-) 23/IL-17 axis is a newly discovered proinflammatory signaling pathway and has been implicated in the pathogenesis of many chronic inflammatory and immune disorders. Here we investigated whether the IL-23/IL-17 axis was present and functional in the lesions of oral lichen planus (OLP), a chronic inflammatory disease affecting the oral mucosa. Using immunohistochemistry and quantitative PCR, we found that the subunits of IL-23 and IL-17 were overexpressed in OLP lesions than in normal oral mucosa tissues. In addition, the expressions of IL-23 and IL-17 are positively correlated in reticular OLP tissues. Results from in vitro studies revealed that exogenous IL-23 could increase the percentage of Th17 cells and IL-17 production in the CD4+T cells from reticular OLP patients. Furthermore, we also found that exogenous IL-17 could significantly enhance the mRNA expressions of β-defensin-2, -3, CCL-20, IL-8, and TNF-α, but not β-defensin-1, CXCL-9, -10, -11, CCL-5, and IL-6 in human oral keratinocytes. Taken together, our results revealed an overexpression pattern and selectively regulatory roles of IL-23/IL-17 axis in the OLP lesions, suggesting that it may be a pivotal regulatory pathway in the complex immune network of OLP lesions.
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