Preeclampsia (PE) is a pregnancy associated disorder that affects 5-8% of pregnancies and is a major cause of maternal, fetal, and neonatal morbidity and mortality. Hallmark characteristics of preeclampsia are new onset hypertension after 20 weeks gestation with or without proteinuria, chronic immune activation, fetal growth restriction, and maternal endothelial dysfunction. However, the pathophysiologic mechanisms that lead to the development of preeclampsia are poorly understood. Recent data from studies of both clinical and animal models demonstrate an imbalance in the subpopulations of CD4+ T cells and a role for these cells as mediators of inflammation and hypertension during pregnancy. Specifically, it has been proposed that the imbalance between two CD4+ T cell subtypes, regulatory T cells (TRegs) and T-helper 17 cells (Th17s), is involved in the pathophysiology of preeclampsia. Studies from our laboratory highlighting how this imbalance contributes to vasoactive factors, endothelial dysfunction and hypertension during pregnancy will be discussed in this review (Fig 1). Therefore, the purpose of this review is to highlight hypertensive mechanisms stimulated by inflammatory factors in response to placental ischemia, thereby elucidating a role for inflammation in the pathophysiology of PE.