CLEC1B and acute respiratory distress syndrome: Another mechanism of pulmonary endothelium protection by platelets was uncovered in the murine model of ARDS and involves platelet receptor CLEC-2 which, by activation of its ligand podoplanin (expressed by inflammatory alveolar macrophages), inhibited the pro-inflammatory phenotype of these macrophages and protected against lung injury [146] (Fig. 4).