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目的探讨系统性红斑狼疮(SLE)T淋巴细胞穿孔素基因启动子区域DNA甲基化状态及其在发病机制中的作用。方法分离9例活动期SLE患者和7例正常人对照外周血CD4~+与CD8~+T细胞,并分别提取DNA。采用亚硫酸氢钠-测序法对CD4~+与CD8~+T细胞穿孔素基因启动子区域DNA甲基化水平进行检测。结果在穿孔素基因启动子区域,正常对照组CD4~+T细胞平均甲基化水平显著高于CD8~+T细胞(P<0.05)。活动期SLE患者CD4~+T细胞平均甲基化水平显著低于正常对照组(P<0.05),而CD8~+T细胞与正常对照组的差异则无统计学意义(P>0.05)。结论活动期SLE患者的CD4~+T淋巴细胞的穿孔素基因启动子区域处于低甲基化状态。
Objective To investigate the DNA methylation status of perforin gene promoter region in systemic lupus erythematosus (SLE) T lymphocytes and its role in pathogenesis. Methods CD4 + and CD8 + T cells from peripheral blood of 9 active SLE patients and 7 normal controls were isolated and DNA was extracted separately. The DNA methylation level of perforin gene promoter in CD4 ~ + and CD8 ~ + T cells was detected by sodium bisulfite-sequencing method. Results In perforin gene promoter region, the average level of CD4 ~ + T cells in normal control group was significantly higher than that in CD8 + T cells (P <0.05). The average level of CD4 ~ + T cells in active SLE patients was significantly lower than that in normal controls (P <0.05), while there was no significant difference between CD8 + T cells and normal controls (P> 0.05). Conclusion The perforin gene promoter region of CD4 ~ + T lymphocytes in active SLE patients is in a hypomethylated state.