Aberrant positioning of trophoblast and lymphocytes in the feto-maternal interface with pre-eclampsia

Pregnancy represents the growth of an allograft where fetal trophoblast cel ls evade immune rejection and invade maternal tissue. There should be a bal ance between fetal trophoblast and maternal immune-responsive cells and alt erations in the proportion of these cells may relate to pregnancy disorders . To test this, the decidual tissue of placental bed biopsies was examined and trophoblast cells and lymphocytes were quantified morphometrically; spi ral arteries were classified as unchanged, transformed or affected by acute atherosis. Normal pregnancy (n=19) was characterized by the transformation of about one half of all spiral arteries within the placental bed. We foun d that 40% of all lymphocytes were CD56(+) uterine NK cells and 60%, CD3(+) T-lymphocytes; about 30% of these were CD8(+) T cells. Intrauterine growth retardation in the context of preeclampsia (n=15) was accompanied by reduc ed trophoblast numbers within smaller and more tortuous arteries and an inc rease in the proportion of CD56(+) uterine NK cells and CD8(+) T lymphocyte s in the decidua (70% of all CD3+ cells). In the case of pre-eclampsia with out fetal growth retardation (n=14) no increase in CD56(+) uterine NK cells was seen, while CD8(+) T lymphocytes were significantly increased compared with the normal level (50% of all CD3(+) cells). Fetal growth retardation is associated with poor transformation of spiral arteries and characterized by an increase of uterine NK cells. Symptoms of pre-eclampsia are independ ently associated with an increase in the cytotoxic T subset of decidual lym phocytes. Pre-eclampsia and related fetal growth retardation are seemingly caused by an enhancement of the maternal cytotoxic defence against the feta l allograft.