Ballesteros, Iván Cuartero, María Isabel Lizasoain, Ignacio Moro, María A
Neutrophils scan for activated platelets to initiate inflammation. [artículo] - Science (New York, N.Y.), 2014 - 346(6214):1234-8.
Formato Vancouver:
Sreeramkumar V, Adrover JM, Ballesteros I, Cuartero MI, Rossaint J, Bilbao I et al. Neutrophils scan for activated platelets to initiate inflammation. Science. 2014 Dec 5;346(6214):1234-8.
PMID: 25477463
PMC4280847
Contiene 23 referencias
Immune and inflammatory responses require leukocytes to migrate within and through the vasculature, a process that is facilitated by their capacity to switch to a polarized morphology with an asymmetric distribution of receptors. We report that neutrophil polarization within activated venules served to organize a protruding domain that engaged activated platelets present in the bloodstream. The selectin ligand PSGL-1 transduced signals emanating from these interactions, resulting in the redistribution of receptors that drive neutrophil migration. Consequently, neutrophils unable to polarize or to transduce signals through PSGL-1 displayed aberrant crawling, and blockade of this domain protected mice against thromboinflammatory injury. These results reveal that recruited neutrophils scan for activated platelets, and they suggest that the neutrophils' bipolarity allows the integration of signals present at both the endothelium and the circulation before inflammation proceeds.
Neutrophils scan for activated platelets to initiate inflammation. [artículo] - Science (New York, N.Y.), 2014 - 346(6214):1234-8.
Formato Vancouver:
Sreeramkumar V, Adrover JM, Ballesteros I, Cuartero MI, Rossaint J, Bilbao I et al. Neutrophils scan for activated platelets to initiate inflammation. Science. 2014 Dec 5;346(6214):1234-8.
PMID: 25477463
PMC4280847
Contiene 23 referencias
Immune and inflammatory responses require leukocytes to migrate within and through the vasculature, a process that is facilitated by their capacity to switch to a polarized morphology with an asymmetric distribution of receptors. We report that neutrophil polarization within activated venules served to organize a protruding domain that engaged activated platelets present in the bloodstream. The selectin ligand PSGL-1 transduced signals emanating from these interactions, resulting in the redistribution of receptors that drive neutrophil migration. Consequently, neutrophils unable to polarize or to transduce signals through PSGL-1 displayed aberrant crawling, and blockade of this domain protected mice against thromboinflammatory injury. These results reveal that recruited neutrophils scan for activated platelets, and they suggest that the neutrophils' bipolarity allows the integration of signals present at both the endothelium and the circulation before inflammation proceeds.
