Building upon existing evidence of macrophage-mediated cytotoxicity in spontaneous abortion (45), our research elucidates mechanistic insights by identifying a novel positive feedback loop: M1-Mφ-derived signals (notably CXCL9) suppress ZEB1 expression, resulting in CCL2 upregulation in trophoblasts, which recruits additional M1-Mφ to the maternal-fetal interface. Here, CXCL9 is linked to abortion.