Infections with Plasmodium falciparum during pregnancy lead to the accumula
tion of parasitized red blood cells (infected erythrocytes, IEs) in the pla
centa. IEs of A falciparum isolates that infect the human placenta were fou
nd to bind immunoglobulin G (IgG). A strain of P. falciparum cloned for IgG
binding adhered massively to placental syncytiotrophoblasts in a pattern s
imilar to that of natural infections. Adherence was inhibited by IgG-bindin
g proteins, but not by glycosaminoglycans or enzymatic digestion of chondro
itin sulfate A or hyaluronic acid. Normal, nonimmune IgG that is bound to a
duffy binding-like domain beta of the P. falciparum erythrocyte membrane p
rotein 1 (PfEMP1) might at the IE surface act as a bridge to neonatal Fc re
ceptors of the placenta.