作者: L. R. Languino , A. Duperray , K. J. Joganic , M. Fornaro , G. B. Thornton
关键词: Fibronectin 、 Cell biology 、 Cell adhesion molecule 、 Vitronectin 、 Fibrinogen binding 、 Biology 、 Intercellular Adhesion Molecule-1 、 Fibrinogen 、 Cell adhesion 、 Molecular biology 、 CD18
摘要: Although primarily recognized for its role in hemostasis, fibrinogen is also required competent inflammatory reactions vivo. It now shown that promotes adhesion to and migration across an endothelial monolayer of terminally differentiated myelomonocytic cells. This process does not require chemotactic/haptotactic gradients or cytokine stimulation the endothelium specific association with intercellular molecule 1 (ICAM-1) on endothelium. Among other adhesive plasma proteins, fibronectin fails increase binding leukocytes endothelium, transendothelial migration, whereas vitronectin but migration. The fibrinogen-mediated leukocyte could be inhibited by a peptide from gamma-chain sequence N117NQKIVNL-KEKVAQLEA133, which blocks ICAM-1. interaction new anti-ICAM-1 monoclonal antibodies did affect ICAM-1-CD11a/CD18 recognition, thus suggesting site ICAM-1 may structurally distinct regions previously implicated leukocyte-endothelium interaction. Therefore, vascular cell receptors sufficient initiate (i) increased (ii) These two processes are earliest events immune responses contribute atherosclerosis.