reticulocytebinding

Reticulocyte binding refers to the molecular interactions by which certain parasites, notably malaria-causing Plasmodium species, attach to reticulocytes—the immature red blood cells released from bone marrow—before or during invasion. Reticulocytes display a different surface protein repertoire than mature erythrocytes, including receptors such as the transferrin receptor (CD71), which can influence parasite tropism. The term is often used to describe ligand–receptor interactions that confer preferential invasion of reticulocytes by some Plasmodium strains.

In Plasmodium vivax, invasion is strongly biased toward reticulocytes, and reticulocyte-binding proteins (PvRBP1, PvRBP2, and related members) are implicated in recognizing reticulocyte surface determinants. In Plasmodium falciparum, invasion is generally broader across erythrocyte ages, but the parasite expresses erythrocyte-binding-like ligands and reticulocyte-binding protein homologs that mediate attachment to specific erythrocyte receptors such as glycophorins and basigin, influencing invasion efficiency rather than strict reticulocyte restriction.

The binding process is typically part of a multi-step invasion sequence, starting with initial contact, tight binding, reorientation, and active merozoite entry, with receptors and ligands providing specificity. Understanding reticulocyte binding has implications for malaria biology, parasite host range, and vaccine development, as blocking these interactions could reduce parasite invasion.

Other pathogens and research contexts may use the term to describe reticulocyte-specific adhesion beyond malaria, but in most scientific usage it refers to the reticulocyte-targeting invasion step of Plasmodium. See also reticulocytes, erythrocyte invasion, PvRBP, RH proteins, EBA, and Duffy antigen receptor for chemokines.