Kalinderis Michail1, Kalinderi Kallirhoe2, Papanikolaou Alexis3
1Department of Obstetrics and Gynecology, Princess Royal University hospital, Orpington, United Kingdom
2Department of General Biology, Aristotle University of Thessaloniki, Medical School, Thessaloniki, Greece
31st Department of Obstetrics and Gynecology, Aristotle University of Thessaloniki, Medical School, Papageorgiou hospital, Thessaloniki, Greece
Correspondence: Papanikolaou Alexis, 1st Department of Obstetrics and Gynecology, Aristotle University of Thessaloniki, Medical School, Papageorgiou hospital, Thessaloniki, Greece, E – mail: email@example.com
Preeclampsia is a pregnancy – specific syndrome associated with increased maternal and fetal morbidity and mortality. The development of preeclampsia occurs in two stages including reduced placental invasion, followed by the activation of endothelial cells and the release of various factors leading to the clinical manifestations of this syndrome. The initial trigger for the incomplete trophoblast invasion in the maternal decidua is still unknown, however the role of the immune system is believed to be of great importance. According to recent data, the pathogenesis of preeclampsia may arise from the interaction between the killer immunoglobulin – like receptors (KIR) of the natural killer (NK) cells of a pregnant woman and the major histocompatibility complex (MHC) of the developing embryo. This review analyses current data regarding the possible association of the NK – MHC system with preeclampsia.
Keywords: preeclampsia, NK cells, KIR receptors, HLA – C2 gene