The Inflammatory Landscape of Pregnancy: Maternal–Fetal Immunity, Basis for Disease, and Targeted Treatments

Inflammation is a normal and essential feature of pregnancy, supporting implantation, placental development, and parturition. When dysregulated, however, inflammatory pathways contribute to major obstetric complications such as preeclampsia, fetal growth restriction (FGR), and preterm birth, which account for substantial maternal and perinatal morbidity and mortality. This review synthesizes current understanding of the maternal–fetal immune interface, examines how inflammation contributes to pregnancy disorders, and explores therapeutic strategies that link pathogenic mechanisms to targeted interventions. The placenta functions as an active immunological hub, coordinating innate and adaptive immune responses to maintain tolerance while protecting against infection. In preeclampsia and FGR, excessive activation—driven by inflammasome signaling, Th1/Th17 polarization, and altered natural killer and macrophage function—impairs placental perfusion, promotes antiangiogenic pathways, and induces systemic endothelial dysfunction. Established therapies, including low-dose aspirin, low-molecular-weight heparin, and antenatal corticosteroids, aim to mitigate inflammation and optimize fetal outcomes, while adjunctive strategies target oxidative stress, nutritional deficits, and the maternal microbiome. Emerging approaches such as cytokine-targeted biologics, inflammasome inhibitors, and mesenchymal stem cell therapies show promise but require rigorous evaluation of safety and efficacy. A deeper understanding of placental immunology and inflammatory signaling is essential to develop precision therapies. Future research should prioritize biomarker validation, pathway-specific interventions, and equitable implementation to reduce inflammation-driven pregnancy complications.