THE IMMUNOLOGICAL ASPECTS OF PREECLAMPSIA

Abstract

The pathogenesis of preeclampsia remains uncertain; nevertheless, endothelial dysfunction, aberrant angiogenesis, trophoblastic invasion, and insufficient remodeling of the spiral artery have been recognized as significant factors. The appropriate remodeling of the spiral artery into dilated, elastic, and low-resistance blood capillaries facilitates an unobstructed delivery of oxygen and nutrients to the fetus. This necessitates the appropriate infiltration of extravillous trophoblasts and the substitution of maternal endothelial cells. Inappropriate activation of the innate immune system and persistent inflammation might result in placental malfunction or inadequate maternal vascular adaptation, hence contributing to the onset of preeclampsia. Immune cells are essential for effective implantation and the formation of the maternal-fetal interaction. Nonetheless, immunological dysregulation and inflammation contribute to the onset of preeclampsia. The decidua contains several types of immune cells, including distinct subtypes of T cells, B cells, NK cells, and macrophages. During a healthy pregnancy, these cells are controlled to facilitate fetal tolerance; nevertheless, they may become disordered, leading to inflammation, oxidative stress, and endothelial dysfunction, as observed in preeclampsia. The etiology of preeclampsia is multifaceted; nonetheless, therapies aimed at the immune system has therapeutic potential. Consequently, comprehending the interplay between the innate and adaptive immune systems in facilitating maternal-fetal tolerance is essential for the advancement of innovative therapeutic strategies for hypertensive diseases during pregnancy.