Maternal-placental immune dialogue.

Immune interactions at the maternal-fetal interface revealed by passive immunization studies (Bondarenko et. al., J. Immunol. 2008 (in press) with anti-Mamu-AG, a placenta-specific MHC class I molecule. Evidence is lacking to support a role in preventing an anti-fetal response (grey), but effector mechanisms (red arrows) suggest a positive role in placental growth and decidual development which underly fetal growth and maternal-well being (blue arrow). Recent evidence indicates Negative outcomes of disruption of these mechanisms include intrauterine growth restriction, pre-eclampsia, and negative impact on neonatal and adult physiology.

Mamu-AG on villous and extravillous trophoblasts will interact directly, via ligand-receptor interactions, and indirectly, via soluble factors or cell-cell interactions, with decidual NK cells, macrophages, and T cells. At least some of these interactions influence remodeling of maternal spiral arterioles by invading endovascular trophoblasts.