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Choi, E.Y.* ; Chavakis, E.* ; Czabanka, M.A.* ; Langer, H.F.* ; Fraemohs, L.* ; Economopoulou, M.* ; Kundu, R.K.* ; Orlandi, A.* ; Zheng, Y.Y.* ; Prieto, D.A.* ; Ballantyne, C.M.* ; Constant, S.L.* ; Aird, W.C.* ; Papayannopoulou, T.* ; Gahmberg, C.G.* ; Udey, M.C.* ; Vajkoczy, P.* ; Quertermous, T.* ; Dimmeler, S.* ; Weber, C.* ; Chavakis, T.*

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

Science 322, 1101-1104 (2008)

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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.

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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.

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