重度子痫前期患者外周血Th17和Treg细胞变化及意义

目的探讨重度子痫前期(s PE)患者外周血Th17及CD4~+CD25~+Treg细胞变化及意义。方法选取2011-2013年镇江妇幼保健院40例s PE患者及40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ELISA检测血浆IL-17、IL-22、TGF-β和IL-10水平,并分析其与s PE的相关性。结果 s PE患者组外周血Th17细胞水平为(1.21±0.82)%,显著高于健康对照组的(0.74±0.63)%,差异有统计学意义(t=3.45,P=0.002)。s PE患者组外周血CD4~+CD25~+Treg细胞水平为(1.65±0.49)%,显著低于健康对照组的(2.42±0.91)%,差异有统计学意义(t=-4.25,P=0.001)。s PE患者组IL-17、IL-22水平分别为80.03±31.25、60.22±18.32ng/L,高于健康对照组的32.84±17.23、35.24±14.33ng/L,差异有统计学意义(t值分别为10.74、5.89,P均0.01),IL-10、TGF-β水平为26.29±10.31、25.65±11.81ng/L,低于健康对照组的33.24±11.93、48.261±13.85ng/L,差异有统计学意义(t值分别为3.35、6.78,P均0.01)。s PE患者血浆IL-17、IL-22水平与Th17细胞水平呈显著正相关(r=0.69、0.58,P0.01)。结论 s PE患者Th17细胞数量增高,CD4~+CD25~+Treg细胞数量减少,以及相关细胞因子的紊乱在s PE的发病机制中可能起到重要作用。

The imbalance of Th17 and Treg cells in patients with severe pre-eclampsia

Objective To analyze the levels of Th17 and CD4+CD25+Treg cells in peripheral blood of patients with sPE. Meth-ods The percentage of Th17 and CD4+CD25+ Treg cells in peripheral blood were examined by flow cytometry. Plasma cytokines levels were measured by ELISA. Results The percentage of Th17 cells in patients with sPE was higher than that of healthy con-trols (1.21±0.82)% vs (0.74±0.63)%,t=3.447,P=0.002]. The percentage of CD4+CD25+Treg cells in patients with sPE was lower than that of healthy controls (1.65±0.49)% vs (2.42±0.91)%,t=-4.25,P=0.001]. Plasma levels of IL-17,IL-22 in sPE patients were 80.03±31.25、60.22±18.32ng/L,and in the control group were 32.84±17.23、35.24±14.33ng/L,respectively,they were signifi-cantly different between the two groups (t=10.74、5.89,all P<0.01). However,IL-10 and TGF-βlevels were markedly decreased in sPE patients compared with controls (26.29±10.31、25.65±11.81ng/L vs 33.24±11.93、48.261±13.85ng/L,t=-3.35、6.78,all P<0. 01). IL-17、IL-21 had positive correlation with Th17 cells (r=0.69、0.58,respectively,all P<0.01) in sPE patients. Conclusion This study suggests that the imbalance of Th17 cells and CD4+CD25+Treg cells,the disorder of related cytokines are important in the pathogenesis of sPE.