The placenta provides a remarkably selective barrier that allows nutrition and immune factors to transfer to the developing fetus, while restricting the passage of potentially harmful molecules. Among the components of the maternal immune system that enter the fetal compartment, IgG antibodies transfer at high concentrations beginning around midgestation,7 culminating in circulating IgG levels in the newborn that exceed those in maternal circulation owing to neonatal FC receptor–mediated active transport across the placenta. This IgG, which is entirely maternal in origin, is thought to provide the newborn with a transient, protective immunity based on the environmental exposures of the mother until the child is capable of mounting an adaptive immune response. However, in cases of maternal autoimmunity, IgG that recognizes self-proteins also crosses the placenta and can interfere with fetal development as in maternal myasthenia gravis, which can lead to transient neonatal myasthenia gravis8 and, in rare cases, the often fatal disorder arthrogryposis multiplex congenita.9 While such conditions are relatively uncommon and the offending IgG are cleared from the infant's circulation within the first 6 months of life, situations where IgG alters important developmental processes can lead to permanent defects. For example, in some cases of neonatal lupus erythematosis,10 characteristic maternal antibodies, which bind to the ribosomal Ro ribonucleoprotein, prevent proper heart formation in the developing fetus, thereby requiring corrective surgery in the newborn.