Objective. Cellular adhesion and differentiation molecules (CAMs) may play a role in the recruitment and retention of inflammatory cells into rheumatoid arthritis synovial tissue (RA ST). In order to determine if certain CAMs are up‐regulated in RA ST compared with normal ST, we studied the distribution of intercellular adhesion molecules (ICAMs) 1, 2, and 3 in ST. We also studied the MS‐1 antigen since it is preferentially expressed on discontinuous endothelia, such as those found in RA ST; MS‐1 is also expressed differentially upon cytokine activation of cells in vitro or in pathologic conditions in situ. Thus, we postulated a possible similarity between MS‐1 and ICAM‐1 expression in inflamed ST. Methods. Immunohistochemical analysis was used to determine the distribution of ICAMs and MS‐1 in ST from 10 patients with RA, 10 with osteoarthritis (OA), and 4 normal individuals. Results. ICAM‐1 expression was found on significantly more RA ST endothelial cells compared with normal cells, as well as on RA ST macrophages and lining cells. ICAM‐2, also found on endothelial cells, showed no differential staining pattern. ICAM‐3 was present on RA ST macrophages and lining cells as well as on some RA and OA endothelial cells. The MS‐1 antigen was present on most RA and OA ST endothelia, lining cells, and macrophages. ICAM‐1 expression and MS‐1 expression in the lining layer were positively correlated in both RA and OA. Conclusion. ICAM‐1, while found mainly on endothelial cells, is up‐regulated on RA ST macrophages and lining cells, suggesting a role for these cells in the infiltration and tissue damage seen in the RA ST. ICAM‐3, which is present mainly on normal resting leukocytes but not on normal endothelium, is expressed by some diseased ST leukocytes and endothelial cells. MS‐1 is also found on the RA ST specialized, fenestrated endothelium, on macrophages, and in the lining layer. These results suggest that the differential expression of ICAMs and MS‐1 in RA ST compared with normal ST might play a special role in the pathogenesis of RA.