Abstract
Antiphospholipid antibodies (aPL) are autoantibodies that target phospholipid-binding proteins, such as β2 glycoprotein I (β2GPI), and can induce thrombosis systemically, as well as increase the risk of obstetric complications such as recurrent miscarriage and preeclampsia. Due to the expression of β2GPI by placental trophoblasts, aPL readily target the maternal-fetal interface during pregnancy and many studies have investigated the deleterious effects of aPL on placental trophoblast function. This review will focus on studies that have examined the effects of aPL on the production and modification of extracellular vesicles (EVs) from trophoblasts, as EVs are a key mode of feto-maternal communication in both normal and pathological pregnancy. A more comprehensive understanding of the effects of aPL on the quantity and cargo of EVs extruded by the human placenta may contribute to our current knowledge of how aPL induce both systemic and obstetric disease.
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