Abstract
BACKGROUND: Recurrent spontaneous abortion (RSA) is characterized by the failure of a pregnancy with the same partner 2 or more consecutive times. Although the precise etiology often remains elusive. Immune dysfunction plays a critical role in RSA. METHODS: This study utilized bibliometric analysis to explore research trends and hotspots in the immune dysfunction associated with RSA over the past 2 decades. By analyzing 823 papers from the Web of Science database published between January 15, 2004, and January 15, 2024, via VOSviewer and CiteSpace, we identified significant findings in this field. RESULTS: Research has focused predominantly on immune cell dysfunction, particularly involving T cells, B cells, NK cells, and macrophages. The leading contributors to this research are China, the United States, and the United Kingdom, with key institutions including Rosalind Franklin University of Medicine and Science and Fudan University. CONCLUSIONS: This study highlights the pivotal role of immune cells at the maternal-fetal interface and calls for ongoing research to elucidate the complex mechanisms of immune-related RSA and to discover potential therapeutic targets. The core immune mechanism underlying RSA primarily involves the overactivation of NK cells and the dysfunction of Treg cells, leading to an imbalance in immune tolerance at the maternal-fetal interface. Dysregulation of Th1/Th2 cytokines, along with a localized inflammatory microenvironment - such as chronic endometritis - further exacerbates this process. Future research should integrate immunophenotypic analysis with targeted therapeutic approaches, such as modulating NK cell activity or enhancing Treg function, to improve pregnancy outcomes in patients with RSA.