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Plugging the leaks

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It has been known for over 20 years that vascular leakage in inflammation is dependent on neutrophils. The identification of the permeability-enhancing activity produced by neutrophils provides clues to the development of anti-inflammatory drugs with a new mechanism of action (pages 1123–1127).

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Figure 1: At a site of inflammation, a neutrophil is activated by a chemoattractant (yellow circle), and adheres to an endothelial cell through β2 integrins (green heterodimers on neutrophil surface; for example, leukocyte function associated molecule-1 (LFA-1)) becoming engaged to endothelial ligands such as intracellular adhesion molecule-1 (ICAM-1).

Bob Crimi

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Authors and Affiliations

  1. Department of Biomedical Engineering and Cardiovascular Research Center University of Virginia Health Sciences Center, Charlottesville, Virginia, USA

    Klaus Ley

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  1. Klaus Ley
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Ley, K. Plugging the leaks. Nat Med 7, 1105–1106 (2001). https://doi.org/10.1038/nm1001-1105

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  • DOI: https://doi.org/10.1038/nm1001-1105

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