Abstract
Preeclampsia is a hypertensive, proteinuric disease that affects 5-10% of all pregnancies and is a leading cause of maternal and perinatal morbidity/mortality (Soto et al., J Matern Fetal Neonatal Med 25: 498-507, 2011). The primary treatment for preeclampsia still is delivery of the fetus and placenta. The underlying mechanisms remain elusive. One possibility is inadequate uterine angiogenesis/vascularity (decidualization) at the time of implantation (Torry et al., Am J Reprod Immunol 51: 257-268, 2004). Here, we review evidence for dysregulation of decidual natural killer (dNK) cells, which secrete important angiogenic factors during decidualization, as a contributing factor in preeclampsia.