Novel clearance mechanisms of platelets

Abstract

Purpose of review: Blood platelets are involved in primary and secondary hemostasis and thus maintain the integrity of the vasculature. They circulate with an average lifespan of 5-9 days in humans. Thus, the body must generate and clear platelets daily to maintain normal physiological blood platelet counts. Known platelet clearance mechanisms include antibody-mediated clearance by spleen macrophages, as in immune thrombocytopenia, and platelet consumption due to massive blood loss.

Recent findings: New concepts in the clearance mechanisms of platelets have recently emerged. New evidence shows that platelets desialyted due to chilling or sepsis are cleared in the liver by macrophages, that is Kupffer cells, as well as hepatocytes, through lectin-mediated recognition of platelet glycans. On the contrary, platelet-associated antibodies normalize the clearance of platelets in a mouse model for Wiskott-Aldrich syndrome.

Summary: The goal of this review is to summarize the latest findings in platelet clearance mechanisms with a focus on lectin-mediated recognition of platelet glycans. Transfusion medicine and treatments of hematopoietic disorders associated with severe thrombocytopenia may benefit from a better understanding of these mechanisms.

Figures

Fig. 1. Platelet clearance pathways

Legend: Platelets bearing incomplete glycans are recognized by either liver macrophages or hepatocyte lectins, which leads to their clearance. IgG-coated platelets are phagocytized by both the Fc and complement receptors in the spleen. IgGs may recognize both amino acid and glycan residues. On the other hand, the binding of immune complexes, e.g. IgAs, to platelets prevents their rapid clearance.