Abstract
Preeclampsia (PE) manifested by hypertension and proteinuria complicates 3% to 8% of pregnancies and is a leading cause of fetal-maternal morbidity and mortality worldwide. It may lead to intrauterine growth restriction, preterm delivery, and long-term sequelae in women and fetuses, and consequently cause socioeconomic burden to the affected families and society as a whole. Balanced immune responses are required for the maintenance of successful pregnancy. Although not a focus of most studies, decidual cells, the major resident cell type at the fetal-maternal interface, have been shown to modulate the local immune balance by interacting with other cell types, such as bone marrow derived-immune cells, endothelial cells, and invading extravillous trophoblasts. Accumulating evidence suggests that an imbalanced innate immunity, facilitated by decidual cells, plays an important role in the pathogenesis of PE. Thus, this review will discuss the role of innate immunity and the potential contribution of decidual cells in the pathogenesis of PE.