It is unclear whether the podoplanin-CLEC-2 axis limits sepsis through parallel mechanisms, namely (i) the activation of platelets; (ii) the interaction with podoplanin on inflammatory macrophages increasing platelet-macrophage aggregation and bacterial trapping, and (iii) controlling the inflammatory response via a macrophage-dependent mechanism and thereby allowing efficient macrophage recruitment to the site of infection. This evidence concerns the gene CLEC1B and Sepsis.