The malaria parasite Plasmodium falciparum utilizes molecules present on th
e surface of uninfected red blood cells (RBC) for rosette formation, and a
dependency on ABO antigens has been previously shown. In this study, the an
tirosetting effect of immune sera was related to the blood group of the inf
ected human host. Sera from malaria-immune blood group A (or B) individuals
were less prone to disrupt rosettes from clinical isolates of blood group
A (or B) patients than to disrupt rosettes from isolates of blood group O p
atients. All fresh clinical isolates and laboratory strains exhibited disti
nct ABO blood group preferences, indicating that utilization of blood group
antigens is a general feature of P. falciparum resetting. Soluble A antige
n strongly inhibited rosette formation when the parasite was cultivated in
A RBC, while inhibition by glycosaminoglycans decreased. Furthermore, a sol
uble A antigen conjugate bound to the cell surface of parasitized RBC. Sele
ctive enzymatic digestion of blood group A antigen from the uninfected RBC
surfaces totally abolished the preference of the parasite to form rosettes
with these RBC, but rosettes could still form. Altogether, present data sug
gest an important role for A and B antigens as coreceptors in P. falciparum
resetting.