We know that the infant expresses homozygous antigens inherited from the father, but what molecules or special signaling pathways block the maternal immune system from rejecting the fetus is still poorly understood by scientists. From the immunological point of view, the fetus is a homozygous graft for the mother, and the fetus will spend nearly ten months in the mother’s body without the maternal immune system rejecting the embryo of the homozygous graft and protecting it from normal development until delivery, which is the only exception to the law of immunology, indicating the existence of a very complex immune response and immune tolerance mechanism of the mother to the embryo. The key site of maternal-fetal immune regulation is the maternal-fetal interface of the placenta. The presence of trophoblasts, immunoreactive cells and cytokines at the maternal-fetal interface plays a key role in the establishment of immune tolerance. Currently, research on the cell biology and molecular immunology of the maternal-fetal interface has become a hot topic in reproductive medicine research. The essence of maternal-fetal immunomodulatory mechanisms, i.e. tolerance of the maternal immune system to embryonic antigens, involves immune tolerance at the maternal-fetal interface and tolerance of maternal immune cells to embryonic antigens. It involves a complex regulation at three levels: recognition of alloantigens, proliferation and memory of immunologically active cells, and immune effects. It is a delicate and complex regulatory process involving the expression of certain specific antigens by trophoblast cells, the inhibition of the activation of metaphase immunoreactive cells, and the execution of specific immune tolerance functions through direct and indirect dialogue between mother-fetus. Trophoblasts at the maternal-fetal interface are of embryonic origin and are the only embryonic cells that come into contact with the maternal meconium and the immunologically active cells therein, and are recognized once in contact, thus playing a crucial role in maternal-fetal immune tolerance. The trophoblast cells of the extravillous cells express a non-classical histocompatibility-like molecule named HLA-G, which is an immune tolerance molecule. Trophoblast cells are protected from natural killer cells in the mother’s body as long as they present the HLA-G molecule. Coincidentally, trophoblast cells are somewhat similar in composition to lymphocytes and cross-react with each other’s corresponding antibodies, hence the term “trophoblast-lymphocyte cross-reactive antigen” (TLX). This is a homozygous allotypic antigen with individual differences between the couple and the mother-fetus, which stimulates the production of a protective blocking antibody that acts with the TLX antigen to protect both the fetus and the placenta from maternal killer T lymphocytes, and another antibody named anti-unique antibody that directly blocks the receptors of maternal killer T lymphocytes and negatively regulates their biological function, causing the maternal immune system to lose its ability to respond to the fetus. The immune system is incapable of attacking the fetus. If this unique type of network loses its regulatory role, the immune protective function becomes impaired and can lead to early pregnancy failure. When we connect these facts, it makes a lot of sense. The fetus is another person parasitic to itself for the mother. After conception, the woman’s body carries out a battle to protect and reject the fetus, in order to prevent her immune system from attacking the fetus, the essence of which is the ability to establish maternal immune tolerance to embryonic antigens, which undergoes a delicate and complex regulatory process that revolves around the expression of specific antigenic molecules in the cells of the trophectoderm, the functional expression of the maternal immune system, especially the immunologically active cells in the meconium, during the The maternal immune tolerance to embryonic antigens is induced through complex and refined molecular physiological interventions starting from the “peri-implantation period”, and then further maintained and strengthened through the regulation of the unique type-anti-unique type network, allowing the fetus, a natural allograft, to survive in a well immunized mother until full term delivery. The fetal allograft survives in the immunocompetent mother until full-term delivery.