Blood monocytes from patients with RA exhibited a greater binding to monolayers of umbilical cord vein endothelium than monocytes from control subjects (mean 42% increase; p < 0.01). When control monocytes were added to TNF or IL-1 treated endothelium their adhesion was enhanced (mean 24% increase; p < 0.05), whereas the number of monocytes from RA patients binding to TNF or IL-1 treated monolayers was less than that adhering to untreated endothelial cells (mean 22% inhibition; p < 0.02). The surface expression of CD11b/CD18 on RA monocytes was increased and pretreatment of normal and RA cells with an anti-CD18 monoclonal antibody inhibited their attachment to untreated and cytokine-treated endothelial cells. Normal blood monocytes activated with LPS demonstrated an enhanced binding to untreated cultures (mean 23% increase; p < 0.05) and an inhibited attachment to cytokine-treated endothelial cells. This study suggests that blood monocytes in RA may be activated and that this property modifies the attachment of these cells to normal and "inflammatory" endothelium.