In particular, we hypothesized the following: (a) in the course of bacterial sepsis, PF4 binds to polyanionic sequences on the surface of aerobic bacteria, forming an antigenic complex that induces early formation of IgG-IgA-IgM directed against PF4-GAGs complexes; and (b) the binding of IgA-IgG-IgM to PF4-GAGs activates platelets, prompting the generation of PF4+PMPs expressing PF4 on their surface with a specific modality. Here, PF4 is linked to bacterial infectious disease with sepsis.