Blood platelets are capable of interacting with monocytes and macrophages and of enhancing various functions of these cells, which are believed to play a role in thrombosis and inflammation. An increase in the uptake of oxidised low density lipoprotein (LDL), in the synthesis of procoagulant tissue factor, thrombospondin and leukotrienes, as well as stimulation of oxygen radical production by platelets has been described (1-5). In circulating blood, a substantial proportion of monocytes was found to be associated with platelets, but the pathophysiological significance of such platelet-monocyte conjugates is not yet clear (6,7). Immigration of monocytes into the arterial intima and their differentiation into macrophages are initial steps in the development of an atherosclerotic lesion (8). During differentiation, there is a tremendous increase in the activity and secretion of the enzyme PAF acetylhydrolase (PAF = platelet-activating factor = 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) (9,10), and there is some evidence that this enzyme may contribute to the development of atherosclerosis. It cleaves PAF, and the remaining lyso-PAF is chemotactic for monocytes (11). Furthermore it also acts on oxidised low density lipoproteins and enhances their uptake into macrophages (12,13). We were therefore interested in investigating whether platelets may modulate the differentiation of monocytes into macrophages and the activity of PAF acetylhydrolase.