补体系统在复发性流产中的研究进展  被引量:3

Disorder of Complement System in Recurrent Spontaneous Abortion

在线阅读下载全文

作  者:赵小萱 张蕊[1] 李娜[2] 陈璐[2] 李大智 冯晓玲[2] ZHAO Xiao-xuan;ZHANG Rui;LI Na;CHEN Lu;LI Da-zhi;FENG Xiao-ling(Heilongjiang University of Chinese Medicine, Harbin 150040,China;Department of Gynecology, First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin 150040, China)

机构地区:[1]黑龙江中医药大学,哈尔滨150040 [2]黑龙江中医药大学附属第一医院妇科

出  处:《国际生殖健康/计划生育杂志》2018年第3期238-242,251,共6页Journal of International Reproductive Health/Family Planning

基  金:国家自然科学基金(81574014;81373673)

摘  要:复发性流产是世界性医学难题,其中免疫因素所致的原因不明复发性流产是当前研究者关注的焦点。补体系统作为固有免疫的重要组成部分,在妊娠过程中发挥着复杂而精细的调控作用。一定程度的补体成分激活对于妊娠过程中胎儿及妊娠附属物的正常发育是必需的,然而在母胎界面上补体系统的过度激活可通过影响胎盘发育、介导炎症损伤,调节特有免疫系统等途径导致胚胎丢失。因此,补体系统失调或过度活化是复发性流产的风险因素。本文对补体系统对正常妊娠的支持及病理激活状态下导致复发性流产的病理机制研究进展进行综述,以期为今后提供可行的免疫治疗方向。The unexplained recurrent miscarriage is a research hotspot in the worldwide medicine,and the immune factors of recurrent abortion have been presently focused.The complement system,as an important component of innate immunity,plays a complex and delicate role in pregnancy.A certain extent of activation of complement components is necessary for the normal development of the fetus and pregnancy appendages during pregnancy.The excessive activation of complement system on the maternal fetal interface can lead to embryo loss by the multiple mechanisms of placental development defect,inflammatory injury,and disorder of specific cellular immune.Therefore,dysfunction or excessive activation of the complement system is a risk factor for recurrent miscarriage.In this review,we reviewed the study progress of complement system in normal pregnancy and recurrent spontaneous abortion,in order to provide a feasible reference for the immunotherapy of recurrent miscarriage.

关 键 词:补体系统蛋白质类 流产 习惯性 补体C3 补体C5 抗体 抗磷脂 免疫 细胞 综述 

分 类 号:R714.21[医药卫生—妇产科学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象