Pregnancy is characterized by mild systemic immunosuppression and inflammation. Traditionally, the fetal–maternal interface was likened to a graft–host interaction. It is becoming more apparent that pregnancy is now a co-dependent, regulatory interaction between the mother and developing fetus. The placenta actively produces and secretes various immunomodulatory factors to prevent rejection of the histoincompatible fetus by the innate and adaptive maternal immune system. Indeed, maternal immune recognition of the fetus occurs throughout uncomplicated pregnancies, and activated CD8+T cells are present at the maternal–fetal interface. Apoptosis is induced in these cells by the FASL-expressing EVT cells. Immunological tolerance at the maternal–fetal interface requires tight temporal regulation between the immune and vascular networks, involving multiple mechanisms. These mechanisms perform a balancing act to regulate trophoblast invasion. Indeed, angiogenesis and trophoblast invasion are immunologically active processes; rather than ‘escaping’ maternal recognition, the fetus harnesses maternal immune surveillance mechanisms to facilitate survival and growth.