The role of the maternal immune system in the regulation of XXXX birthweight.

@entity1 @entity9371 @entity16304 @entity3885 @entity1592 @entity18698
@entity1 birthweight is subject to stabilizing selection. Large babies are at risk of obstetric complications such as @entity3885 , which endangers both mother and @entity1 . Small babies are also at risk with reduced survival. Fetal growth requires remodelling of maternal spiral arteries to provide an adequate maternal blood supply to the placenta. This arterial transformation is achieved by placental trophoblast cells, which invade into the uterine wall. Under-invasion is associated with @entity1592 ; but if invasion is excessive large babies can result. A growing body of evidence suggests that this process is controlled by interactions between killer-cell immunoglobulin-like receptors (KIRs) expressed on maternal uterine natural killer cells (uNK) and their corresponding human leukocyte antigen-C ( @entity18698 ) ligands on invading trophoblast. Mothers with the @entity9371 AA genotype and a fetus with a paternal HLA-C2 allele tend to have small babies, because this combination inhibits cytokine secretion by uNK. Mothers with the activating @entity16304 gene and an HLA-C2 fetus are more likely to have large babies. When @entity16304 binds to HLA-C2 this increases secretion of cytokines that enhance trophoblast invasion. We conclude that specific combinations of the highly polymorphic gene systems, @entity9371 and @entity18698 , contribute to successful reproduction by maintaining birthweight between two extremes.
