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Serum sickness nephritis was induced in Fischer rats by preimmunization and repeated immunization with chicken egg albumin. This experimental model is characterized by marked accumulation of monocytes/macrophages (MO) and deposition of immune complexes (IC) in glomeruli during the inflammatory stage and, thereafter, the advancement to glomerulosclerosis. The correlations between glomerular tissue damage, MO participation, intercellular adhesion molecule-1 (ICAM-1) expression and IC deposition were analyzed during the long-term disease process. The grade of ICAM-1 expression was well correlated with MO accumulation and IC deposition, and its distribution was observed on the glomerular endothelial layer, mesangium, and along the parietal epithelial layer of the Bowman's capsule. It is suggested that glomerular MO accumulation is largely affected by the ICAM-1 expression on glomeruli and, underneath such adhesion molecules, MO may play a role in subendothelial or mesangial migration, mesangial cell activation, inducing sclerosis and monocytic-epithelial crescent formation.