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Science. 2008 Nov 14;322(5904):1101-4. doi: 10.1126/science.1165218.

Del-1, an endogenous leukocyte-endothelial adhesion inhibitor, limits inflammatory cell recruitment.

Author information

1
Experimental Immunology Branch, Center for Cancer Research, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD, USA.

Erratum in

  • Science. 2009 Aug 21;325(5943):946.

Abstract

Leukocyte recruitment to sites of infection or inflammation requires multiple adhesive events. Although numerous players promoting leukocyte-endothelial interactions have been characterized, functionally important endogenous inhibitors of leukocyte adhesion have not been identified. Here we describe the endothelially derived secreted molecule Del-1 (developmental endothelial locus-1) as an anti-adhesive factor that interferes with the integrin LFA-1-dependent leukocyte-endothelial adhesion. Endothelial Del-1 deficiency increased LFA-1-dependent leukocyte adhesion in vitro and in vivo. Del-1-/- mice displayed significantly higher neutrophil accumulation in lipopolysaccharide-induced lung inflammation in vivo, which was reversed in Del-1/LFA-1 double-deficient mice. Thus, Del-1 is an endogenous inhibitor of inflammatory cell recruitment and could provide a basis for targeting leukocyte-endothelial interactions in disease.

PMID:
19008446
PMCID:
PMC2753175
DOI:
10.1126/science.1165218
[Indexed for MEDLINE]
Free PMC Article

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