Placental immunoregulation.

Mammalian gestation is complex and varies widely among species, but the embryonic contribution to the maternal-fetal interface, the trophoblast, remains constant. Alloantigen and stage/tissue specific antigens are present on the trophoblast in low concentration and often in locations inaccessible to maternal immune effectors. Nonetheless, pregnancy does prime the mother for humoral immunity; cell-mediated responses are more difficult to demonstrate. The placenta appears to be an efficient block to cellular traffic into the fetus; the placental barrier to specific antibody has been established, but its efficiency is controversial. Nonspecific, local, active suppression mediated by lymphoid cells within the decidua is apparently an important concomitant of successful gestation. Yet there is evidence that an ongoing immune response is beneficial to pregnancy, allowing an increase in placental size in response to growth-promoting lymphokines while blocking graft-rejection mechanisms. Thus it appears that immunoregulation at the maternal-fetal interface is complex, and no single mechanism can account for the success of the "fetal allograft".