Del-1, an Endogenous Leukocyte-Endothelial Adhesion Inhibitor, Limits Inflammatory Cell Recruitment

Author:

Choi Eun Young12345,Chavakis Emmanouil12345,Czabanka Marcus A.12345,Langer Harald F.12345,Fraemohs Line12345,Economopoulou Matina12345,Kundu Ramendra K.12345,Orlandi Alessia12345,Zheng Ying Yi12345,Prieto DaRue A.12345,Ballantyne Christie M.12345,Constant Stephanie L.12345,Aird William C.12345,Papayannopoulou Thalia12345,Gahmberg Carl G.12345,Udey Mark C.12345,Vajkoczy Peter12345,Quertermous Thomas12345,Dimmeler Stefanie12345,Weber Christian12345,Chavakis Triantafyllos12345

Affiliation:

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

2. Molecular Cardiology, Department of Internal Medicine III, J. W. Goethe University, Frankfurt, Germany.

3. Department of Neurosurgery, Charite Universitätsmedizin, Berlin, Germany.

4. Institute for Molecular Cardiovascular Research, RWTH University Hospital, Aachen, Germany.

5. Laboratory of Cellular Oncology, Center for Cancer Research, NCI, NIH, Bethesda, MD, USA.

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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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