The immunoregulatory disturbances in the pathogenesis of pre-eclampsia

Abstract

Abstract Pre-eclampsia is one of the most common obstetric disorders that occurs in 5-10% of pregnant women. The signs and symptoms of this syndrome appear during the second or the third trimester of pregnancy. It manifests mainly as hypertension and proteinuria. This disorder is a leading cause of mortality and morbidity among not only mothers but also newborns. Although many researchers have carried out studies concerning pre-eclampsia, the etiology of the syndrome is still unknown. It was found that pre-eclampsia as a placenta disorder develops in two stages. During the first stage there is too shallow invasion of cytotrophoblast into spiral arteries. The second stage of the disease relies on the production of some substances from ischaemic placenta which can induce the damage of endothelium. There are some observations which suggest that the syndrome is an immunological disorder. For example, there is a protective effect of sperm exposure which can support an immunological etiology. There are also evidences that the length of sexual cohabitation before pregnancy is one of protective factors. It has been suggested that the cause of pre-eclampsia is an insufficient maternal tolerance to paternal antigens. It has been found out that pre-eclampsia is a "Th1 phenomenon" what means that in feto-maternal unit and in peripheral blood of pre-eclamptic women there is a predominance of Th1 response over Th2 immunity. Moreover, the deficiency of T regulatory cells has been observed in pre-eclampsia. There was also underlined that the alterations in the function of natural killer (NK) cells, macrophages and dendritic cells (DCs) play an important role in the development of pre-eclampsia