We evaluated the expression of the cell-adhesion molecules (CAM) that might be involved in liver-associated lymphocyte (VU) contacts with other sinusoidal cells and/or be responsible for natural-killer(NK)-and lymphokine-activated killer(LAK) activity in patients with liver metastasis. The LAL population was isolated by sinusoidal high-pressure lavage from partial hepatectomies obtained from patients operated for metastases (n = 13) and benign liver tumors (n = 9). Surface expression of the beta-2-integrin chains (CD I I a, CD I I b, CD I I c and CDI 8), and the beta-I-integrin chains (CD49b, CD49d. CD49f and CDZP), as well as that of members of the immunoglobulin superfamily (CD2, CD54. CD56 and CD58), were analyzed by one-or two-color flow cytometry. Quantitative and qualitative differences were observed in both groups of patients in the expression of CAM between LAL and peripheral blood lymphocytes (PBL). I A L were characterized by an increase in the percentage of CD I I b-, CD49b-. CD49d-, CD54-. CD56-and CD58-positive cells in comparison with PBL. Fluorescence values for CD2, CD I I a, CD 18 and CD56 were higher in LAL than in PBL. Moreover, the population expressing these antigens of differentiation presented a bimodal distribution (dim and bright): in LAL, as opposed to PBL, the percentage of cells with a bright phenotype was greater than of those with a dim one. The increase in CAM expression on LAL could be due to the influence of the liver sinusoidal micro-environment. Results were more unexpected for the comparison between benign and malignant tumors. No difference was found in CAM expression on LAL between these 2 categories. Consequently, it cannot be this factor that explains the decrease in LAK activity of LAL in patients with metastasis.