Abstract: Recurrent spontaneous abortion (RSA) has complex etiologies, including embryonic chromosomal abnormalities, maternal immune factors, prethrombotic states, and uterine anatomical anomalies. Currently, the pathogenesis of RSA remains incompletely elucidated, with placental trophoblast dysfunction considered a key factor contributing to pregnancy failure. Recent studies have demonstrated that non-coding RNA (ncRNA) are stably expressed at the maternal-fetal interface and regulate the proliferation, apoptosis, invasion, and metastasis of trophoblast immune cells. The ncRNA can directly modulate target gene expression or influence the occurrence and progression of RSA through competitive endogenous RNA (ceRNA) regulatory networks, providing novel targets for researchers exploring the pathogenesis of RSA. Additionally, ncRNA mediate intercellular interactions via vesicular transport, offering new insights into their regulatory mechanisms. Due to their tissue specificity and expression stability, ncRNA are promising as novel biomarkers for RSA and other pregnancy-related disorders. This review summarized the regulatory roles of ncRNA in the immune mechanisms underlying the occurrence and development of RSA based on multiple domestic and international studies.