国际妇产科学杂志 ›› 2026, Vol. 53 ›› Issue (1): 103-107.doi: 10.12280/gjfckx.20251156

• 产科生理及产科疾病: 综述 • 上一篇    下一篇

抗磷脂综合征致复发性流产的免疫炎症血栓机制

赵佳润, 郑舒畅, 王一迪, 王成霞, 何军琴()   

  1. 100026 首都医科大学附属北京妇产医院/北京妇幼保健院
  • 收稿日期:2025-10-15 出版日期:2026-02-15 发布日期:2026-03-11
  • 通讯作者: 何军琴 E-mail:hejunqin@ccmu.edu.cn
  • 基金资助:
    国家自然科学基金(82074477);首都卫生发展科研专项(首发2024-2-2114)

Immune-Inflammatory Thrombotic Mechanism of Recurrent Spontaneous Abortion Caused by Antiphospholipid Syndrome

ZHAO Jia-run, ZHENG Shu-chang, WANG Yi-di, WANG Cheng-xia, HE Jun-qin()   

  1. Beijing Obstetrics and Gynecology Hospital, Capital Medical University/Beijing Maternal and Child Health Care Hospital, Beijing 100026,China
  • Received:2025-10-15 Published:2026-02-15 Online:2026-03-11
  • Contact: HE Jun-qin E-mail:hejunqin@ccmu.edu.cn

摘要:

复发性流产(recurrent spontaneous abortion,RSA)的病因复杂多样,其中免疫性疾病抗磷脂综合征(antiphospholipid syndrome,APS)作为血栓形成的高危因素,主要通过免疫炎症血栓机制导致不良妊娠结局的发生。APS主要通过抗磷脂抗体(antiphospholipid antibody,aPL)启动免疫炎症血栓级联反应,即蜕膜自然杀伤细胞、蜕膜巨噬细胞及调节性T细胞功能失衡,肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)、γ干扰素(interferon-γ,IFN-γ)等促炎因子过度释放,损害血管内皮,进而激活Janus激酶(Janus kinase,JAK)-信号转导及转录活化因子(signal transducer and activator of transcription,STAT)、核因子κB(nuclear factor-κB,NF-κB)等信号通路激活补体、损伤血管内皮,促进局部血栓形成,导致母胎界面免疫微环境失衡。因此,基于对免疫炎症血栓病理机制的深入解析,综述APS致RSA的发生机制及临床治疗进展,旨在为未来的研究提供参考,为实施新的诊疗方案提供新的切入点,为药物靶向诊疗RSA合并APS提供理论依据与临床实践参考。

关键词: 流产,习惯性, 抗磷脂综合征, 细胞因子类, 免疫, 血栓炎症

Abstract:

The etiology of recurrent spontaneous abortion (RSA) is complex and diverse. Among them, the immune disease antiphospholipid syndrome (APS), as a high-risk factor for thrombosis, mainly leads to adverse pregnancy outcomes through the immune-inflammatory thrombosis mechanism. APS mainly initiates the immune-inflammatory thrombosis cascade reaction through antiphospholipid antibodies (aPLs). That is, there is a functional imbalance among decidual natural killer cells, decidual macrophages, and regulatory T cells, and an excessive release of pro-inflammatory factors such as tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ), which damage the vascular endothelium. Subsequently, it activates signaling pathways such as Janus kinase (JAK)-signal transducer and activator of transcription (STAT) and nuclear factor-κB (NF-κB), activates the complement system, damages the vascular endothelium, promotes local thrombosis, and leads to an imbalance in the immune microenvironment at the maternal-fetal interface. Therefore, based on the in-depth analysis of the pathological mechanism of immune-inflammatory thrombosis, this paper reviews the occurrence mechanism and clinical treatment progress of RSA caused by APS, aiming to provide reference for future research, a new entry point for implementing new diagnosis and treatment plans, and a theoretical basis and clinical practice reference for targeted drug diagnosis and treatment of RSA complicated with APS.

Key words: Abortion, habitual, Antiphospholipid syndrome, Cytokines, Immunity, Thromboinflammation