At the site where the placenta implants there is intermingling of fetal trophoblast cells with maternal tissues. Uterine natural killer (uNK) cells are defined by the high expression of the surface marker CD56 so they are designated CD56superbright. NK cells are not a feature of the myometrium so the behavior of trophoblast in the deeper part of the uterus is independent of their influence. A further potential site where maternal immune cells can interact with endovascular trophoblast is in the spiral arteries in the decidua basalis. All uNK cells express high levels of the inhibitory receptor CD94/NKG2A whose ligand is HLA-E. HLA-G is a non-classical HLA class I molecule that was identified and found to be expressed by trophoblast cells nearly 20 years ago. The overall conclusion is that the local immunity in the human implantation site is an unusual one that is reflected in the cell types present.

At the time of the discovery of the physiological changes of spiral arteries in the pregnant uterus, Brosens and colleagues suggested that these changes result from the destructive action of the invading trophoblasts on the vascular smooth muscle and the elastic membrane. This chapter reiterates the main findings regarding the successive spiral artery remodeling steps. It seems appropriate to relate the time-course of the vascular remodeling process to the new insights in uteroplacental flow changes during this pregnancy period. In preeclampsia, trophoblast-associated remodeling is restricted to decidual spiral arteries throughout the placental bed. Spiral artery conversion is obviously important for safeguarding an adequate maternal blood supply to the placenta. Deep trophoblast invasion and spiral artery remodeling of the inner 'junctional zone' myometrium is a feature of normal human pregnancy, while in preeclampsia and maybe in other pregnancy complications this process may be seriously impaired.