Neutrophils in inflamed blood vessels adopt a polarized morphology and begin crawling on endothelial cells before their extravasation into the tissues. In Science, Hidalgo and colleagues describe interactions between activated platelets and neutrophils that provide a checkpoint for neutrophilic function during inflammation. Polarized neutrophils cluster the P-selectin ligand PSGL-1 on their uropods, which causes platelet accumulation at their trailing edge. Blocking this interaction blunts the polarization of other receptors on neutrophils, including the integrin Mac-1 and the chemokine receptor CXCR2, and alters their crawling activity. Notably, loss of the interaction of platelets with luminal neutrophils also blocks the release of neutrophil nets and lessens tissue damage in several models of inflammation. Thus, neutrophils seem to utilize activated platelets as a 'go' signal to enter inflamed tissues.

Science 346, 1234–1238 (2014)