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- W2010681857 abstract "Rejection continues to be one of the major causes of allograft loss in renal transplantation. Immunological rejection is mediated by neutrophils, macrophages, NK cells, and T cells infiltrating the transplanted organ [ 1 ]. Another active participant in this process is the vascular endothelium. In the inflammatory response there is a loss of permeability by endothelial contraction, cytoskeletal reorganization, or endothelial injury that produces optimal adhesion between endothelial and leukocyte molecules [2]. Adhesion of leukocytes to endothelial cells is a regulated process that involves multiple sequential steps [3] (Figure 1). The initial step is rolling of leukocytes along the venule wall mediated by the selectin family of adhesion molecules [4]. There are three selectins: L-selectin located in leukocytes, P-selectin on platelets and on stimulated endothelium, and E-selectin on stimulated endothelium [5,6]. The second step is strong adhesion between leukocytes and endothelium mediated by binding of integrins to members of the immunoglobulin superfamily on endothelial cells. The key players in this phase of recruitment for the neutrophils are the p2 integrins LFA-1 and Mac-1, and for monocytes and lymphocytes also the p integrin VLA-4 [7]. LFA-1 and Mac-1 interact with ICAM-1 and VLA-4 binds to VCAM-1 present on the surface of the endothelium [8]. Strong adhesion depends upon the increased expression of" @default.
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- W2010681857 title "Adhesion molecules and the mechanisms of kidney rejection. New approaches to therapy" @default.
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