目的:探讨重度子痫前期(sPE)患者外周血及胎盘组织中Th17及CD4+CD25+Treg细胞水平变化及意义。方法:选取20例sPE患者及20名健康对照者,采用流式细胞术检测外周血单个核细胞中Th17及CD4+CD25+Treg细胞水平,采用QRT-PCR检测外周血和胎盘组织中孤儿核受体RORγt mRNA和Treg细胞转录因子Foxp3 mRNA的表达水平并分析其与sPE的相关性。结果:sPE患者组外周血Th17细胞水平为(1.16±0.78)%显著高于对照组的(0.68±0.35)%,外周血CD4+CD25+Treg细胞水平为(1.65±0.49)%显著低于对照组的(2.42±0.91)%。外周血RORγt mRNA表达水平为0.19±0.06高于对照组的0.14±0.03,Foxp3+mRNA表达水平为0.07±0.03低于对照组的0.13±0.03,差异有统计学意义(P<0.01)。胎盘组织RORγt mRNA表达水平为3.76±1.85高于对照组的2.05±1.02,Foxp3+mRNA表达水平为0.83±0.51低于对照组1.51±0.81,差异有统计学意义(P<0.01)。结论:sPE患者Th17细胞数量增高,CD4+CD25+Treg细胞数量减少,在sPE的发病机制中可能起到重要作用。 Objective: To investigate the changes and significance of Th17 and CD4 + CD25 + Treg cells in peripheral blood and placenta of patients with severe preeclampsia (sPE). Methods: 20 cases of sPE patients and 20 healthy controls were selected. The levels of Th17 and CD4 + CD25 + Treg cells in peripheral blood mononuclear cells were detected by flow cytometry. The orphan nuclear receptors in peripheral blood and placenta were detected by QRT-PCR The expression level of RORγt mRNA and Treg cell transcription factor Foxp3 mRNA were analyzed and their correlation with sPE was analyzed. Results: The level of Th17 cells in peripheral blood of patients with sPE was significantly higher than that of control (1.16 ± 0.78)% vs (0.68 ± 0.35)%, while the level of CD4 + CD25 + Treg in peripheral blood was (1.65 ± 0.49)% Group (2.42 ± 0.91)%. The level of RORγt mRNA in peripheral blood was 0.19 ± 0.06, which was significantly higher than that in control group (0.14 ± 0.03). The expression level of Foxp3 + mRNA in control group was 0.07 ± 0.03, which was significantly lower than that in control group (0.13 ± 0.03) (P <0.01). The level of RORγt mRNA in placenta was 3.76 ± 1.85 higher than 2.05 ± 1.02 in control group, and the level of Foxp3 + mRNA in control group was 0.83 ± 0.51, lower than that of control group (1.51 ± 0.81) (P <0.01). Conclusion: The increased number of Th17 cells and the decrease of CD4 + CD25 + Treg cells in sPE patients may play an important role in the pathogenesis of sPE.