国际妇产科学杂志 ›› 2013, Vol. 40 ›› Issue (6): 525-529.

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CD4+T细胞在原因不明复发性流产中的研究进展

王文娟,林其德   

  1. 264000 山东青岛大学医学院附属烟台毓璜顶医院生殖中心(王文娟);上海交通大学医学院附属仁济医院妇产科(林其德)
  • 收稿日期:1900-01-01 修回日期:1900-01-01 出版日期:2013-12-15 发布日期:2013-12-15
  • 通讯作者: 王文娟

The Role of CD4+T Cells in Unexplained Recurrent Spontaneous Abortion:an Update

WANG Wen-juan,LIN Qi-de   

  1. Reproductive Medical Center,Affiliated Yuhuangding Hospital,Qingdao University Medical School,Yantai 264000,China(WANG Wen-juan);Department of Obstetrics and Gynecology,Renji Hospital,School of Medicine,Shanghai Jiao Tong University,Shanghai 200001,China(LIN Qi-de)
  • Received:1900-01-01 Revised:1900-01-01 Published:2013-12-15 Online:2013-12-15
  • Contact: WANG Wen-juan

摘要: 正常妊娠有赖于母体对胚胎半同种抗原的免疫耐受,一旦免疫耐受失衡,将导致免疫排斥、免疫攻击从而导致自然流产,原因不明复发性流产被认为与母胎免疫耐受失衡有关。CD4+T在同种异体急性排斥反应中发挥重要作用,根据所分泌的细胞因子不同,CD4+T 细胞分为Th1、Th2、调节性T细胞(Treg)及新近发现的Th17细胞。早期研究发现母体外周血、母胎界面CD4+T细胞增高与复发性流产密切相关。随免疫耐受机制研究的不断深入,母胎免疫耐受的研究历经Th1/Th2平衡到Treg的免疫负调控作用,再到Th17/Treg平衡。综述CD4+T细胞在原因不明复发性流产中的研究进展。

关键词: 流产, 复发性, Th1细胞, Th2细胞, T淋巴细胞, 调节性, Th17细胞

Abstract: The human gestation is a semi-allograft and hence antigenically foreign to the mother. Therefore, the process of implantation may include mechanisms to prevent allograft rejection, but once the immunological tolerance becomes imbalanced, pathological pregnancy, such as spontaneous abortion could occur. Unexplained recurrent spontaneous abortion (URSA) is thought to be caused by immunological rejection of the fetus by the mother. CD4+ T cells which include Th1, Th2, regulatory T cells (Treg) and Th17 cells, play important roles in allograft rejection. Maternal peripheral blood and decidual CD4+ T cells augmentation have been implicated in URSA. Mechanisms of immune tolerance is in the deepening,from the Th1/Th2 immune balance to the negative regulation of Treg cells. Recently, the Th17/Treg balance, has been described to paly an important role in the immunological rejection. In this paper the role of CD4+ T cells in URSA is reviewed.

Key words: Abortion, recurrent, Th1 cells, Th2 cells, T-lymphocytes, regulatory