Comparative studies of placentation and immunology in non- @entity1 primates suggest a scenario for the evolution of deep trophoblast invasion and an explanation for XXXX pregnancy disorders.

@entity1 @entity17056 @entity17055 @entity831 @entity4839 @entity1592 @entity1468 @entity74 @entity18698
Deep trophoblast invasion in the placental bed has been considered the hallmark of @entity1 pregnancy. It occurs by two routes, interstitial and endovascular, and results in transformation of the walls of the spiral arteries as they traverse the decidua and the inner third of the myometrium. Disturbances in this process are associated with @entity74 such @entity1468 . In contrast, trophoblast invasion in Old World monkeys occurs only by the endovascular route and seldom reaches the myometrium. Recently, it was shown that this pattern is maintained in gibbons, but that the @entity1 arrangement also occurs in @entity831 and @entity17056 . There is an interesting parallel with results from placental immunology regarding the evolution of the major histocompatability complex class I antigen @entity18698 and its cognate receptors. @entity18698 is not present in Old World monkeys or gibbons. It emerged in the @entity17055 and became polymorphic in the lineage leading to @entity17056 , @entity4839 , @entity831 , and @entity1 . Interaction between HLA-C1 and HLA-C2 on the surface of trophoblast and killer immunoglobulin-like receptors (KIRs) expressed by uterine natural killer cells are important regulators of trophoblast invasion. Evolution of this system in great apes may have been one prerequisite for deep trophoblast invasion but seems to have come at a price. The evidence now suggests that certain combinations of maternal genotype for KIRs and fetal genotype for @entity18698 imply an increased risk of @entity1468 , @entity1592 , and recurrent abortion. The fetal genotype is in part derived from the father providing an explanation for the paternal contribution to @entity74 .
