Prenatal mortality due to loss of lymphocyte-promoted endometrial angiogenesis is being investigated as a major cause of litter reductions during pregnancy in pigs. This review discusses immune mechanisms influencing porcine endometrial angiogenesis as well as additional signalling molecules that may play important roles in the compromise of peri-implantation and mid-gestation fetal pig survival. These include dendritic cells, signalling molecules such as toll-like receptors, chemokines and ficolins. Together these cells and molecules regulate immune responses and, ideally, protect the mother and prevent immune-based conceptus losses. Dendritic cells were recently shown to be angiogenic. Their tolerogenic role at the maternal-fetal interface coupled with the ability to secrete and respond to angiogenic factors suggests that dendritic cells are the key coordinators of angiogenesis at the porcine maternal-fetal interface. Chemokines coordinate the localization of immune effector and endothelial cells. The balance between pro-angiogenic and anti-angiogenic chemokines is addressed in relation to conceptus viability. Ficolins, components of the lectin-mediated complement activation pathway, are used for self/non-self recognition. Together, these components of the immune system could regulate lymphocyte- and non-lymphocyte-promoted endometrial angiogenesis to determine conceptus survival.