论文部分内容阅读
目的:探讨动脉粥样硬化(AS)患者外周血CD4 T细胞及调节性T细胞(CD4+CD25high CD127-Treg)比例及功能的变化。方法:选择AS患者(AS组)及健康体检者(健康对照组)各40例,抽取外周静脉血,用流式细胞术测定CD4 T细胞、CD8 T细胞、IFN-γ+CD4 T细胞、IFN-α+CD4 T细胞和CD4+CD25high CD127-Treg细胞比例,以及各自的CD4+CD25high CD127-Treg细胞与CD4 T细胞共培养后,CD4 T细胞增殖能力以及CD4 T细胞分泌炎症因子能力的变化。结果:与健康对照组比较,AS组外周血CD4 T细胞比例及CD4 T/CD8 T比值明显升高、IFN-γ+CD4T及IFN-α+CD4 T细胞比例明显升高(均P<0.05),而CD8 T细胞比例与CD4+CD25high CD127-Treg细胞比例差异无统计学意义(均P>0.05)。健康对照组CD4 T细胞的增殖能力、IFN-γ及IFN-α分泌能力在与CD4+CD25high CD127-Treg细胞共培养后较其单独培养均明显降低(均P<0.05),而AS组CD4 T细胞的以上指标在与CD4+CD25high CD127-Treg细胞共培与单独培养间差异均无统计学意义(均P>0.05)。结论:AS患者外周血CD4+CD25high CD127-Treg细胞功能的丧失,导致外周血CD4 T细胞比例升高、分泌炎症因子能力增强,从而引发AS的炎症状态。
Objective: To investigate the changes of the proportion and function of CD4 T cells and regulatory T cells (CD4 + CD25high CD127-Treg) in peripheral blood of patients with atherosclerosis (AS). Methods: Peripheral venous blood was collected from 40 AS patients (AS group) and healthy subjects (healthy control group), and the levels of CD4 T cells, CD8 T cells, IFN-γ + CD4 T cells, IFN α + CD4 T cells and CD4 + CD25high CD127-Treg cells, as well as their CD4 + CD25high CD127-Treg cells co-cultured with CD4 T cells, CD4 T cell proliferation and CD4 T cell secretion of inflammatory cytokines. Results: The proportion of CD4 T cells and the ratio of CD4 T / CD8 T in AS group were significantly higher than those in healthy control group (P 0.05) , While there was no significant difference in the proportion of CD8 T cells and CD4 + CD25high CD127-Treg cells (all P> 0.05). The proliferation, IFN-γ and IFN-α secretion of CD4 T cells in CD4 (superscript +) CD8 + T cells were significantly decreased in CD4 (superscript +) CD25 + T cells compared with those in CD4 + CD25 + T cells There was no significant difference between the above indexes of cells and those of CD4 + CD25high CD127-Treg cells (all P> 0.05). Conclusion: The loss of CD4 + CD25high CD127-Treg cells in peripheral blood of AS patients leads to an increase in the proportion of CD4 T cells in peripheral blood and an increased ability to secrete inflammatory cytokines, thus triggering the inflammatory state of AS.