LAUSR

Preeclampsia (PE) is a hypertensive disorder that occurs after 20 weeks of gestation, implicating the placenta as a key offender. PE is associated with an imbalance among B lymphocytes, CD4+ T lymphocytes, NK cells and increased inflammatory cytokines. During early onset PE, trophoblast invasion and placentation are impaired, leading to reduced blood flow to the fetus. In all spectrums of this disorder, a shift towards a pro‐inflammatory state where regulatory cells and cytokines are decreased occurs. Specifically, inflammatory CD4+ T‐cells and inflammatory cytokines are increased while CD4+ T regulatory cells (Tregs) and immunosuppressive cytokines such as IL‐4 and IL‐10 are decreased resulting in B cell activation, production of autoantibodies, endothelial dysfunction and hypertension associated with PE. However, the stimulus for these imbalances is unknown and need to be fully understood so that effective treatments that target the pathogenesis of the disease can be designed. Therefore, this review will focus on the pathways involving CD4+, TH1, TH2, Tregs, TH17s, B cells, and NK cells in the pathophysiology of PE.