PERIPHERAL NATURAL KILLER CELLS (CD56) AND PREECLAMPSIA

Abstract

P reeclampsia is the most frequently encountered medical complication of pregnancy. It is characterized by the new onset of hypertension and proteinuria, usually during the last trimester of pregnancy, and is commonly associated with edema and hyper uricemia (Sibai et al., 2005). The placenta plays a central role in the pathogenesis of preeclampsia,as evidenced by the rapid disappearance of clinical signs and symptoms of preeclampsia following delivery of the placenta. Preeclampsia is characterized by widespread systemic vascular endothelial dysfunction and microangiopathy in the mother, but not in the fetus (Karumanchi et al., 2005). Although defective placental trophoblastic invasion and dysfunction of maternal vascular endothelium are significant in the pathogenesis of preeclampsia, maladaptive or altered immune response is also believed to play an important role in this pregnancy disorder. Exaggerated inflammatory response, imbalance of Th1/Th2 cytokine generation (Jonnson et al., 2006), and aberrant interaction of maternal leukocytes and placental trophoblasts at the maternal-fetal interface (Chaouat et al.,2005) are all considered to be the crucial components of the altered immune response during preeclampsia. In preeclampsia, the shift away from type1 responses either fails to occur or is reversed, with increased production of IL-18 and IFN relative to normal pregnancy (Germain et al., 2007). This type1bias can be seen in T cells (Saito et al., 2007) and more predominantly in NK or NK like T (Borzychowski et al., 2005).