It has been proposed that advanced glycosylated end products (AGEs) are involved in the pathogenesis of vascular damages in both type 1 and type 2 diabetes. Furthermore, it has been assumed that AGEs cause an alteration of both expression and activity of cell adhesion molecules which are responsible for migration of circulating cells through the endothelial layer of the vessels. The effect of AGEs on the activity of cell adhesion molecules was studied in our experiments using the homotypic adhesion assay, specific monoclonal antibodies and lymphoid cell lines. It was shown that proteins glycosylated in vitro seemed to increase the percentage of homotypic aggregation of lymphoid cells. This effect was mediated via the interaction between LFA-1 and ICAM-1 which was demonstrated by the fact that specific monoclonal antibodies against these cell adhesion molecules could block the effect of the AGEs. The results obtained reveal that the advanced glycosylated end products activate the function of cell adhesion molecules on lymphoid cells. It can be speculated that the activation of cell adhesion molecules might enhance the direct cellular contacts between the lymphoid cells in the immune response. Moreover, the effect of AGEs might be responsible for an enhanced adhesion of monocytes to endothelial cells and their migration through the vessel wall.