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[Immunological aspects of preeclampsia]
B Leszczyńska-Gorzelak1, D Darmochwał-Kolarz
1Kliniki Połoznictwa i Perinatologii II Katedry Połoznictwa i Chorób Kobiecych AM w Lublinie.
Pre-eclampsia is a common obstetric syndrome affecting about 7-10% of pregnant women. Symptoms of this syndrome: hypertension and impaired renal function appear during the second or third trimester of pregnancy. Despite intensive efforts to find mechanisms and markers induced pre-eclampsia, no specific etiological factor has been identified until now. It is known that pre-eclampsia is a placental disorder developing in two stages. The first lies in the poor placentation with acute atheroma. It seems that abnormal cell adhesion molecule (integrin) expression can contribute to inappropriate invasion of trophoblasts. Furthermore, T helper 1 type cytokines which are present in decidua of patients with pre-eclampsia can alter the trophoblast invasion. Lower expression level of HLA-G molecule in pre-eclamptic placenta can influence on the profile of cytokines which are produced in pre-eclampsia. The second stage of the disease development comprises the consequences of placental ischemia. It has been suggested that TNF-alpha is produced by ischemic placenta and causes endothelial activation. It seems that some types of pre-eclampsia can be autoimmune origin, with the autoantibodies directed against phospholipids, laminin and endothelium. The events leading to pre-eclampsia are not known, but it seems that abnormal activation of the immune system may play a role in the etiology of this disorder.
Pre-eclampsia is a common obstetric syndrome affecting about 7-10% of pregnant women. Symptoms of this syndrome: hypertension and impaired renal function appear during the second or third trimester of pregnancy. Despite intensive efforts to find mechanisms and markers induced pre-eclampsia, no specific etiological factor has been identified until now. It is known that pre-eclampsia is a placental disorder developing in two stages. The first lies in the poor placentation with acute atheroma. It seems that abnormal cell adhesion molecule (integrin) expression can contribute to inappropriate invasion of trophoblasts. Furthermore, T helper 1 type cytokines which are present in decidua of patients with pre-eclampsia can alter the trophoblast invasion. Lower expression level of HLA-G molecule in pre-eclamptic placenta can influence on the profile of cytokines which are produced in pre-eclampsia. The second stage of the disease development comprises the consequences of placental ischemia. It has been suggested that TNF-alpha is produced by ischemic placenta and causes endothelial activation. It seems that some types of pre-eclampsia can be autoimmune origin, with the autoantibodies directed against phospholipids, laminin and endothelium. The events leading to pre-eclampsia are not known, but it seems that abnormal activation of the immune system may play a role in the etiology of this disorder.