The Immunopathology of Preeclampsia

Abstract

Preeclampsia (PE) is a hypertensive disorder of pregnancy characterized by target organ damage, affecting approximately 5% of pregnancies. Complex neuroendocrine alterations, vascular imbalances, excessive oxidative stress, environmental factors, and inappropriate immune responses drive the pathology of this condition. Inadequate remodeling of the uterine spiral arteries serves as a fundamental marker of the disease. PE is heavily mediated by an inflammatory cascade involving complement system activation, decreased tolerogenicity of natural killer (NK) cells, M1 macrophage polarization, and dendritic cell alterations. Furthermore, the disease is characterized by a shift toward Th1, Th17, and Th22 cell populations, alongside a decrease in Th2 and regulatory T (Treg) lymphocytes, significantly increasing the risk of maternal autoimmunity. The disorder also disrupts angiogenesis, alters specialized pro-resolving lipid mediators, and impairs responses to infections. Although advancements in immunological treatments have been made, many therapeutic approaches remain under active investigation.