Placental trophoblast and endothelial cells as target of maternal immune response.

Pregnancy is a unique physiologic condition that guarantees the survival of the semiallogenic embryo during the long period of gestation. The placenta plays a key role in the maintenance of local tolerance and allows the mother to accept the embryo until completion of pregnancy. The complex process of tolerance accompanying the survival of the foetus is controlled at the embryo-maternal interface by factors deriving from decidualized endometrium and from the trophoblast itself. Trophoblasts develop various strategies to evade the damaging attack by the maternal immune response including expression of non-classical MHC class I antigens and of complement regulatory proteins. Also, cytokines released at the feto-maternal interface play an important role in regulating embryo survival controlling not only the maternal immune response but also angiogenesis and vascular remodelling. The delicate equilibrium established between the mother and the foetus can be compromised in pathological condition of pregnancy as a result of humoral and/or cellular response of the mother against trophoblast antigens leading to spontaneous miscarriage. Cytotoxic cells and antibodies to trophoblast and endothelial cells are frequently found in patients with recurrent spontaneous abortion. This review article focuses on the delicate equilibrium established at the feto-maternal interface during pregnancy examining the various strategies devised by the embryo to evade the maternal immune attack, and the pathological conditions in which this equilibrium is compromised leading to serious complications of pregnancy.