View article

Transplacental passage of maternal antibodies was first described in 1895 with the finding of anti-diphtheria toxin antibodies in fetal blood by Fischl and Von Wundscheim. 1 Over the past century, the role of maternally derived antibodies in passive neonatal immunity has been extensively studied, but this protection against infection comes with a price: self-reactive antibodies transferred to the fetus may result in neonatal autoimmunity. The resultant antibody-mediated disease phenotype depends not only on the antigen specificity, titer, and affinity of the antibody transferred, but on the gestational age and underlying health of the newborn, because these factors can influence the transplacental and gastrointestinal acquisition of immunoglobulins from the mother. 2-4

In addition to maternal–fetal antibody transfer, transplacental acquisition and retention of whole maternal cells by the human fetus can occur5-7—a phenomenon previously believed to be impossible. These maternal cells persist and are detectable in healthy individuals for years after birth, 8 signifying a chronic chimeric state termed maternal microchimerism (MMc). In the first half of this chapter, we will review examples of maternal antibody–mediated autoimmunity in the neonate (Table 10-1) and will speculate on hypothetical roles for maternal antibodies in modulating the risk of autoimmune disease. In the second half, we will describe the relationship between MMc and neonatal autoimmune disease, and the role of T regulatory cells in controlling neonatal autoimmunity.