Increased placental villous macrophages in patients with antiphospholipid syndrome exacerbated during preterm...

Antiphospholipid syndrome (APS) during pregnancy is a high-risk condition associated with miscarriage, stillbirth, preeclampsia, fetal growth restriction, and preterm birth resulting from placental insufficiency. However, the immunopathological mechanisms underlying placental dysfunction in APS remain poorly understood. This study aimed to characterize the immune cell profile in placentas from APS patients whose pregnancies required preterm termination due to worsening maternal or fetal conditions.

Placental tissues were collected from patients diagnosed with APS and from gestational age-matched controls. Immunohistochemistry and immunofluorescence analyses were performed to identify and quantify immune cell populations, including macrophages, neutrophils, and lymphocytes. Localization of inflammatory mediators such as interleukin-1β (IL-1β) was also assessed.

APS placentas exhibited a significant increase in CD68⁺ macrophages within the chorionic villi compared with control placentas, whereas macrophage numbers in the intervillous spaces and decidua were unchanged. Immunofluorescence revealed that CD80^- CD163⁺ CD206^- macrophages predominated in the villous stroma of APS placentas, contrasting with control placentas that contained CD80^- CD163⁺ CD206⁺ resident macrophages (Hofbauer cells). Additionally, CD80^- CD163^- CD206^- macrophages were observed aggregating along syncytiotrophoblasts in APS placentas. Neutrophil infiltration was also elevated in APS placentas, although less abundant than macrophages. IL-1β localized beneath syncytiotrophoblasts and around the villous stroma but did not colocalize with macrophages or neutrophils. Both B and T lymphocytes were scarce in APS and control placentas.

These findings indicate that APS placentas exhibit distinct alterations in macrophage populations within the chorionic villi, suggesting a potential role of macrophages in mediating placental pathology.