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Comparative evaluation of the role of the adhesion molecule CD177 in neutrophil interactions with platelets and endothelium

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Abstract

Neutrophil‐specific glycoprotein CD177 is expressed on a subset of human neutrophils and has been shown to be a counter‐receptor for platelet endothelial cell adhesion molecule‐1 (PECAM‐1, CD31). Previous studies have demonstrated that the interaction of CD177 with endothelial PECAM‐1 supports neutrophil transendothelial migration resulting in preferential transmigration of the CD177‐expressing neutrophil subset. As PECAM‐1 is also abundantly expressed on platelets, we addressed a follow‐up suggestion that CD177/PECAM‐1 adhesive interaction may mediate platelet–neutrophil interactions and CD177‐positive neutrophils may have a competitive advantage over CD177‐negative neutrophils in binding platelets. Here, we report that CD177‐positive and CD177‐negative neutrophils do not differ significantly in their capacity to form platelet–neutrophil conjugates as assayed in whole blood and in mixed preparations of isolated platelets and neutrophils. Under flow conditions, neither platelet nor neutrophil activation resulted in preferential binding of platelets to CD177‐expressing neutrophils. Furthermore, no significant difference was found in the ability of both neutrophil subsets to adhere to and migrate across surface‐adherent activated platelets, whereas predominantly CD177‐positive neutrophils migrated across HUVEC monolayers. In addition, we demonstrated that S536N dimorphism of PECAM‐1, which affects CD177/PECAM‐1 interaction, did not influence the equal capacity of the two neutrophil subsets to interact with platelets but influenced significantly the transendothelial migration of CD177‐expressing neutrophils. Thus, CD177/PECAM‐1 adhesive interaction, while contributing to neutrophil‐endothelial cell interaction in neutrophil transendothelial migration, does not contribute to or is redundant in platelet–neutrophil interactions.
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Document Type: Research Article

Publication date: September 1, 2012

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