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