Influences of cerebral stent implantation on CD4+ CD25+ FOXP3+ Treg, Th1 and Th17 cells.
Influences of cerebral stent implantation on CD4+ CD25+ FOXP3+ Treg, Th1 and Th17 cells.
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DOI：
10.1016/j.intimp.2013.07.024
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发表时间：
2013-11
影响因子：
5.6
通讯作者：
Sijia Wang;B. Ni;Kangning Chen;S. Shi
中科院分区：
文献类型：
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作者：
Sijia Wang;B. Ni;Kangning Chen;S. Shi
支架植入术主要用于治疗动脉狭窄。然而，支架支柱的应用和使用会诱发局部和全身炎症，导致顽固性内膜增生。 CD4+T细胞参与动脉狭窄疾病，但CD4+T细胞对支架植入后炎症反应的影响知之甚少。在这项研究中，我们分析了 2011 年 12 月至 2012 年 6 月期间接受颅内或颈部支架植入的 50 名患者的 CD4+T 细胞每种亚型的特征转录因子和促炎细胞因子表达的频率。结果表明，Treg 细胞中特征转录因子/细胞因子产生的频率在支架植入后第一周内降低，并在支架植入后 3 个月恢复到控制水平。然而，我们观察到 Th17 细胞的相反趋势，显示急性期特征转录因子/细胞因子的产生增加，3 个月后恢复到控制水平。在支架植入前后患者的 Th1 细胞中，未观察到特征转录因子/细胞因子表达频率存在显着差异。我们推测调节性T细胞的频率和功能的维持控制着炎症反应，否则炎症反应会在支架植入后诱发急性炎症。
Stent implantation is primarily used for the treatment of artery stenosis. However, the application and use of stent struts induces local and systemic inflammation, leading to intractable neointimal hyperplasia. CD4+T cells are involved in artery stenosis diseases, but little is known about the influence of the CD4+T cells on the inflammation reaction after stent implantation. In this study, we analyzed the frequency of signature transcription factors and proinflammatory cytokine expression from each subtype of CD4+T cells in 50 patients receiving intracranial or cervical stent implantations from December 2011 to June 2012. The results showed that the frequency of signature transcription factor/cytokine production in Treg cells was reduced in the first week and returned to control levels at 3 months after stent implantation. However, we observed opposite trends for Th17 cells, showing increased signature transcription factor/cytokine production during the acute phase, which returned to control levels after 3 months. No significant difference in the frequency of signature transcription factor/cytokine expression was observed in Th1 cells from patients before and after stent implantation. We speculate that the maintenance of the frequency and function of Tregs controls the inflammatory response, which otherwise induces acute inflammation after stent implantation.