The role of immune cells and mediators in preeclampsia

Preeclampsia is a hypertensive disorder of major concern in pregnancy than can lead to intrauterine growth restriction, placental abruption and stillbirth. The pathophysiology of preeclampsia is multifactorial, including both kidney dysfunction and endothelial dysfunction, as the maternal endothelium becomes exposed to placental factors that are released into the circulation and increase systemic levels of vasoconstrictors, oxidative stress, anti-angiogenic factors and inflammatory mediators. In addition, inflammation can lead to insufficient placental perfusion and low birthweight in offspring. Various innate and adaptive immune cells and mediators have been implicated in developing preeclampsia, in which oxidative stress is associated with activating the maternal inflammatory response. Immune cells such as regulatory T cells, macrophages, natural killer cells, and neutrophils are known to have major causative roles in the pathology of preeclampsia. However, the contributions of other immune cells, such as B cells, inflammatory cytokines and anti-angiotensin II type 1 receptor autoantibodies, are also now recognized. Immunological interventions, therefore, have therapeutic potential in this disease. Here, the study provides an overview of the immune responses involved in the pathogenesis of preeclampsia, including the role of innate and adaptive immune cells and mediators.