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Rolling back neutrophil adhesion

Nature Immunology volume 11, pages 282–284 (2010)Cite this article

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Neutrophils and other cells secrete the pentraxin PTX3, which promotes innate immunity by binding to pathogens and activating complement. PTX3 can also limit neutrophil recruitment by inhibiting rolling on P-selectin in inflamed venules.

During inflammation, flowing neutrophils tether to and roll on vascular surfaces by reversible binding of P-, L- and E-selectin to glycosylated ligands1,2. One of the earliest events is mobilization of P-selectin from secretory granules to the surfaces of endothelial cells and platelets after activation by thrombin, complement and other mediators. P-selectin initiates rolling by interacting with the transmembrane mucin PSGL-1 on neutrophils. Rolling permits selectin ligands and chemokine receptors on neutrophils to signal integrin-dependent deceleration, arrest and, ultimately, immigration into infected or injured tissues3. Whereas the mediators that trigger inflammation have been studied extensively, less is known about the mechanisms that limit inflammation. In this issue of Nature Immunology, Mantovani and colleagues report that the pentraxin PTX3, a protein known to augment innate immunity, also dampens neutrophil recruitment in vivo4. PTX3 binds to P-selectin and may limit inflammation by inhibiting the rolling of neutrophils on P-selectin.

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Figure 1: Model for PTX3's paracrine regulation of neutrophil rolling on P-selectin.

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Affiliations

  1. Rodger P. McEver is in the Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.

    Rodger P McEver

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  1. Rodger P McEver
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Correspondence to Rodger P McEver.

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Competing interests

R.P.M. is a cofounder of Selexys, a start-up company that is developing antibody-based inhibitors of selectins or selectin ligans.

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McEver, R. Rolling back neutrophil adhesion. Nat Immunol 11, 282–284 (2010). https://doi.org/10.1038/ni0410-282

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  • DOI: https://doi.org/10.1038/ni0410-282

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