The existence during gestation of an immunological buffer zone at the interface between maternal and foetal tissues.
In mammalian pregnancy the trophoblast normally constitutes an uninterrupted boundary of foetal tissue in immediate contact with maternal tissue, including blood in some species, and is the decisive immunological barrier to rejection of the foetus as an allograft. The ability of the trophoblast to function as a barrier evidently results from its capacity to resist immunological attack by either alloantibody or alloimmune cells and to prevent immunocompetent cells from reaching and damaging the foetus but, as yet, there is no general agreement regarding the means by which it exercises these functions. In view of the dramatic hormonal changes that occur during pregnancy and the undisputed involvement of trophoblast in these endocrine events, the possibility exists of an interaction between the hormones of pregnancy and the immunological phenomena. The present account furnishes evidence that endocrine activity at the maternal surface of the trophoblast, the presumptive site of the immunological frontier between foetus and mother, may be a factor in its local survival at implantation. The placental hormones so far known that are capable of blocking the antigen receptor sites of the mother's lymphocytes and thus preventing the latter from reacting with the foetal antigens are the glycoprotein, human chorionic gonadotrophin (HCG) and the polypeptide hormone, human chorionic somatomammotrophin (HCS) or human placental lactogen (HPL), both of which are specific to the human placenta. The origin of these hormones, their spatial distribution and their probable interaction with placental steroid hormones are discussed. It is argued that the place of highest concentration of these hormones is on the surface of the syncytial microvilli and the adjacent caviolae of the apical plasma membrane, as well as on the surfaces of the persisting cytotrophoblastic cells of the basal plate (cytotrophoblastic shell), the cell islands and the septa-precisely where the immunological challenge of the foetal allograft to the maternal host occurs. An explanation is offered for the continuing production of the voluminous quantities of these hormones during human pregnancy.
D000818:Animals; D000937:Antigen-Antibody Reactions; D006063:Chorionic Gonadotropin / Q000096:biosynthesis / Q000276:immunology*; D010064:Embryo Implantation; D004967:Estrogens / Q000276:immunology; D005260:Female; D006041:Goats; D006064:Gonadotropins, Equine / Q000276:immunology; D006648:Histocompatibility; D006736:Horses; D006801:Humans; D007165:Immunosuppression Therapy; D008214:Lymphocytes / Q000276:immunology; D008253:Macaca mulatta; D008431:Maternal-Fetal Exchange; D010926:Placental Hormones / Q000096:biosynthesis / Q000276:immunology; D011247:Pregnancy; D011374:Progesterone / Q000276:immunology; D014327:Trophoblasts / Q000166:cytology / Q000276:immunology*
D006063:Chorionic Gonadotropin; D004967:Estrogens; D006064:Gonadotropins, Equine; D010926:Placental Hormones; D011374:Progesterone