AP-HP, département d’hématologie biologique, hôpital Necker, Paris, France
HITh, UMR_S 1176, Inserm, université Paris-Saclay, 94270 Le Kremlin-Bicêtre, France
The sialic acid content on the surface of platelets decreases over the course of their life. This process is due to the mechanism of desialylation, involving sialidase enzymes. The absence of sialic acid exposes β-galactose residues, which are considered as senescent antigens. Genes regulating the synthesis and transfer of sialic acid, as well as mechanisms that exacerbate desialylation, are responsible for thrombocytopenia. In this review, we present basic and clinical data from the literature highlighting the important role of platelet sialylation. We also discuss the possibility of measuring platelet β-galactose exposure from a clinical perspective in order to identify patients with certain forms of thrombocytopenia who could benefit from an experimental treatment to suppress sialidase activity.