HE TRANSMISSION of specific immunity from mother to young was first described by Paul Ehrlich in 1892, who observed that the young mice from dams made resistant to toxins were also immune to the same toxins. ~ This immunity was limited in extent and time, and appeared to originate from the selective transfer of maternal antibody. It was soon appreciated that transfer of passive immunity was a physiological phenomenon in mammals, and that the maternally derived antibodies protect the neonate against most common infections? Because the immune system of the mammalian fetus and neonate is not fully developed, this transfer is essential to the survival of the individual as well as the species. The mechanism behind this transfer of passive immunity is not yet fully understood, although much insight has been gained in later years. 3-7 Not only beneficial maternal immunoglobulin G (IgG), but also potentially deleterious antibody will cross the syncytiotrophoblast barrier. Some of these antibodies, such as anti-HLA alloantibodies, appear to be trapped and sequestered within the placenta by binding to HLA antigen or to Fc receptors (FcR) as soluble immune complexes of chorionic nontrophoblastic cells, and do not reach the fetus. This mechanism has recently been reviewed elsewhere. 8 Clinically important exceptions that may escape placental trapping are the transfer of maternal IgG antibodies to fetal erythrocytes, (eg, anti-Rh[D] antibodies), with hemolytic disease of the fetus and newborn as a consequence; or anti-platelet antibodies to fetal thrombocytes (eg, anti-HPAla antibodies), resulting in neonatal alloimmune thrombocytopenia. Another disadvantageous effect of FcR-mediated transfer of IgG is the potential of enhancement of vertical human immunodeficiency virus (HIV) infection through syncytiotrophoblasts where FcRIII appear to be important. 9 Improved