Pre-eclampsia remains a leading cause of maternal and infant morbidity and
mortality. Insufficient invasion of trophoblast cells into the myometrial p
ortions of the spiral arteries is thought to play a crucial role in the dev
elopment of pre-eclampsia. As a consequence, uteroplacental vessels fail to
undergo adaptive changes which are imperative to provide a sufficient bloo
d supply to the placenta. Consecutive placental hypoxia is supposed to caus
e secretion/shedding of still unidentified placental metabolites resulting
in different forms of pregnancy-induced hypertension. This review presents
published data concerning the causes of insufficient trophoblast invasion i
n preeclampsia. Expression of HLA-G by extravillous trophoblast cells seems
to be altered, resulting in activation of the maternal immune system. The
pattern of integrin expression as well as the secretion of proteases is rep
orted to be disturbed, which could lead to a reduced invasive potential of
the trophoblast cells. Recent data indicate a pathophysiological role of NK
-cells and macrophages in the altered trophoblast invasion. In summary, pre
eclampsia seems to be induced by a multifactorial disturbance of trophoblas
t invasiveness which is characterised by reduced invasiveness of the tropho
blast cells themselves and by an activated maternal immune response blockin
g the invasion by the semiallogenic trophoblast.