From an immunological perspective, a normal pregnancy is similar to a successful homozygous semi-allogeneic transfer in that the mother not only does not reject embryos carrying paternal antigens, but also establishes a unique immune microenvironment at the maternal-fetal interface through a refined maternal-fetal dialogue, allowing fetal growth and development in utero until delivery. Thus, maternal-fetal immune regulation can be seen as a central component of the maternal-fetal dialogue, with successful pregnancies actually reflecting maternal immune tolerance to embryonic antigens, while pregnancy failure is mostly associated with abnormal maternal-fetal immune rejection of the embryo (reported in the literature as 80%). The cell composition of the maternal-fetal interface is quite complex and can be broadly classified into three categories according to their origin; the first category is fetal-derived chorionic trophoblasts and extrachorionic trophoblasts that invade the meconium; the second category is medullary-derived immunoreactive cells (NK, DC, MΦ, T, etc.); and the third category is meconium stromal cells and glandular epithelial cells. Cytokines produced by ecdysteroid immunoreactive cells constitute a unique cytokine network that regulates the immune response at the maternal-fetal interface, creating a Th2 type of immune dominance. Regulatory T cells (Treg) are significantly increased in number at the maternal-fetal interface during early pregnancy and are able to suppress the rejection of paternal antigens or alloantigens by maternally activated cells. The proper functioning of trophoblast invasion and proliferation is essential for blastocyst implantation, embryonic development, and the establishment of a proper maternal-fetal relationship. If extravillous trophoblast invasion capacity is inadequate, the spiral arteries retain their contractile function and insufficient blood flows to the intervillous space, leading to the development of pregnancy-related disorders such as recurrent spontaneous abortion (RSA), fetal arrest, and biochemical pregnancy.