Journal
SCIENCE
Volume 346, Issue 6214, Pages 1234-1238Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1256478
Keywords
-
Categories
Funding
- NIH [HL03463, HL085607, HL090676]
- German Research Foundation [ZA428/8-1, ZA428/6-1, SFB 1009-TP A05]
- FP7 Marie Curie from Comunidad de Madrid [ITN-264864, S2010/BMD-2326]
- Japan Society for the Promotion of Science
- Ministerio de Economia y Competitividad (MINECO) [SAF2012-33216]
- Comunidad de Madrid [S2010/BMD-2336, S2010/BMD-2314]
- Ramon y Cajal Fellowship from MINECO [RYC-2007-00697, SAF2009-11037, 2012-31142]
- FP7-People-IRG Program [246655]
- MINECO
- Pro-CNIC Foundation
- Grants-in-Aid for Scientific Research [25251015, 24111001, 24111007] Funding Source: KAKEN
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available