Fig. 2. The role of JAM-A, JAM-B and JAM-C in leukocyte-plateletendothelial cell interactions. Homophilic and heterophilic interactions of JAM-A, JAM-B and JAM-C suggest that various heterotypic cell-cell interactions might be supported by JAMs. Binding of leukocytes to endothelial cells might be supported by integrins LFA-1 and 4ß1 binding to JAM-A and JAM B, respectively, on endothelial cells. Note that the 4ß1-mediated association with JAM-B seems to be enhanced by JAM-C co-expression with 4ß1 on the same leukocyte. Leukocyte binding to endothelial cells might also be mediated by leukocyte JAM-C binding to endothelial JAM-B. Leukocyte adherence to platelet deposits is mediated by the leukocyte integrin Mac-1 binding to JAM-C on platelets. Platelet binding to endothelial cells might be supported by JAM-A homophilic interactions. The associations illustrated in this figure have been shown in different experimental systems. Static cell-substrate adhesion assays with recombinant proteins immobilized on plastic were used to show the interaction between JAM-C and JAM-B (Arrate et al., 2001; Liang et al., 2002), 4ß1 and JAM-B (Cunningham et al., 2002), Mac-1 and JAM-C (Santoso et al., 2002), and JAM-A and JAM-A (Babinska et al., 2002a). Static cell-cell adhesion assays showed the association between LFA-1 and JAM-A (Ostermann et al., 2002), Mac-1 and JAM-C (Santoso et al., 2002) and between JAM-A and JAM-A (Babinska et al., 2002a). An interaction in cell-cell adhesion assays under flow conditions has so far been shown for LFA-1 and JAM-A (Ostermann et al., 2002), as well as for Mac-1 and JAM-C (Santoso et al., 2002).