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外周血Th17及CD4^+CD25^+FoxP3^+调节性T细胞失衡与不明原因反复自然流产的相关性研究 被引量:10

Investigation of the relationship between the imbalance of Th17 cells/CD4^+CD25^+FoxP3^+ regulatory T cells and unexplained recurrent spontaneous abortion
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摘要 目的观察不明原因反复自然流产(URSA)孕妇外周血Th17与CD4+CD25+FoxP3+调节性T细胞比例的变化,探讨Th17/T细胞比例失衡在URSA孕妇发病机制中的作用。方法选择36例URSA孕妇为实验组,健康早孕妇女40例为对照组,应用流式细胞仪检测Th17与CD4+CD25+FoxP3+T细胞的比例,应用ELISA法检测IL-6、TGFβ-和IL-17的水平。结果 URSA孕妇外周血中,CD3+CD8-IL-17+T细胞占CD3+T淋巴细胞的百分比高于对照组,P<0.05;CD4+CD25+FoxP3+T细胞占CD4+T淋巴细胞的百分比明显低于对照组,P<0.05。相关细胞因子测定结果显示,IL-6、IL-17水平在URSA孕妇血清中均明显升高,TGF-β水平在2组间比较,差异无统计学意义。结论外周血Th17与CD4+CD25+FoxP3+调节性T细胞的比例及相关细胞因子数量的异常可能下调母胎免疫耐受功能,参与URSA的发生。 Objective To investigate the changes of Th17/CD4+ CD25+ FoxP3+ regulatory T cells(Treg) ratio within peripheral blood in pregnant women with unexplained recurrent spontaneous abortion and to explore the role of Thl7/Treg imbalance in UR SA. Methods Flow cytometry was used to detect the Thl7 and CD4+ CD25+ FoxP3+ T cells in 36 cases of pregnant women with URSA and 40 healthy pregnant women(control group). The concentrations of serum IL-6, TGF-β and IL-17 of all subjects were tested by enzyme linked immunosorbent assay(ELISA). Results The proportion of CD3+ CD8 IL-17+ cells in total CD3 + T cells of URSA patients was higher than that of control group(P〈0.05) and the proportion of CD4 + CD25+ FoxP3+ T cells in total CD4+ cells was lower in URSA patients,compared with control group(P〈0.05). Among the detected cytokines, concentrations of serum IL-6 and IL-17 were higher in URSA patients as compared with control group(P〈0.05), except TGF-β(P〈0.05). Conclusion This study suggests the abnormality of Th17/CD4+ CD25+ FoxP3+ Treg ratio could down-regulate the immune function of mater nal-fetal tolerance and mediate unexplained recurrent spontaneous abortion possibly through the variances of IL-6 and TGF-β.
出处 《国际检验医学杂志》 CAS 2011年第10期1036-1038,共3页 International Journal of Laboratory Medicine
关键词 流产 自然 T淋巴细胞 调节性 细胞因子类 免疫耐受 abortion, spontaneous T lymphoeytes, regulatory cytokines immune tolerance
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