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      Adhesion molecules in human crescentic glomerulonephritis.

      The Journal of Pathology

      analysis, E-Selectin, Glomerulonephritis, metabolism, pathology, Humans, Immunoenzyme Techniques, Integrins, Intercellular Adhesion Molecule-1, Kidney Glomerulus, chemistry, Vascular Cell Adhesion Molecule-1, Cell Adhesion Molecules

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          The expression of the intercellular adhesion molecule-1 (ICAM-1) and its ligand lymphocyte function associated antigen-1 (LFA-1 or alpha L), the vascular cell adhesion molecule-1 (VCAM-1), endothelial leukocyte adhesion molecule-1 (ELAM-1), and the cellular receptors for extracellular matrix, alpha 1, alpha 2, alpha 3, alpha 5, alpha 6, alpha V, beta 1, and beta 3 integrin subunits, was studied in 28 patients with crescentic glomerulonephritis (GN) related to several mechanisms: four patients with anti-glomerular basement membrane antibodies or anti-GBM disease; 16 with immune complex mediated GN; and eight with pauci-immune GN, associated with vasculitis in four cases. A three-step immunoperoxidase technique was used on sections obtained from frozen renal biopsies. At the initial stage of evolution of the lesions, all the cells of the crescents expressed the beta 1, beta 3, alpha 1, alpha 3, and alpha V subunits of integrins, ICAM-1, and VCAM-1, and some cells expressed the alpha 2, alpha 5, alpha 6, and alpha L subunits of integrins along the plasma membrane. At a later stage, when the crescents were fibrocellular, alpha 3 and alpha 1 subunit expression was polarized, localized mainly in front of the extracellular matrix. In fibrotic crescents, the alpha 2, alpha 5, alpha 6, and alpha L chains were no longer detected, and VCAM-1 and ICAM-1 expression was decreased. VCAM-1 and ELAM-1 appeared on endothelial cells of peritubular capillaries in relation to the appearance of infiltrating inflammatory cells. The results of this study show that several adhesion molecules were expressed on cells forming crescents and were modified during crescent evolution; that these molecules were up-regulated on endothelial cells in relation to the severity of the inflammatory response; and that whatever the mechanism of the glomerulonephritis, adhesion molecule expression was identical. It can be postulated that adhesion molecules play a role in crescentic glomerulonephritis. Better knowledge of these molecules in human glomerulonephritis may open the way to a new therapeutic approach.

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