The functions of different populations of peripheral blood monocytes in the course of an inflammatory reaction are presently not fully understood. In particular, the mechanisms for their specific recruitment to an inflammatory site are not yet known. We investigated a dexamethasone (Dex)-inducible monocyte subtype and its adhesion to either unstimulated or lipopolysaccharide (LPS)- or interferon (IFN)-gamma-stimulated human umbilical vein endothelial cells (HUVEC). The Dex-induced monocytes were characterized by the expression of the surface glycoprotein RM3/1. It was found that pretreatment of monocytes with Dex increased their adhesion to unstimulated and stimulated HUVEC. This increase in adhesion was paralleled by the expression of the RM3/1 surface molecule. Treatment with cyclosporin A (CsA) caused a down-regulation of the RM3/1 density per cell by 67% and also decreased adhesion to HUVEC. In contrast, the expression of other adhesion molecules remained unaffected by Dex or CsA treatment. Treatment of Dex-induced monocytes with antibodies against RM3/1, CD11a, CD11b, CD11c, CD14 and CD18 resulted in suppression of adhesion to stimulated HUVEC by 46%, 18%, 17%, 12%, 25% and 15%, respectively. Antibodies to the known adhesion molecules on endothelial cells (vascular cell adhesion molecule-1, E-selectin) did not block adhesion of Dex-induced monocytes. However, the combination of antibodies to RM3/1 and CD14 inhibited adhesion to LPS-stimulated HUVEC by 74%. These effects were also seen on IFN-gamma-stimulated HUVEC, where adhesion of Dex-induced monocytes was blocked with antibodies to RM3/1 + CD14 by 63%. From this, it is concluded that the RM3/1-molecule is a novel surface molecule that contributes to the adhesion of cortisone-induced monocytes to LPS or cytokine-stimulated endothelial cells.