Recent advances in cellular immunology have resulted in completely new perspectives on the treatment of human diseases that have presumed autoimmune aetiology. There is now an increasing focus on the specific molecular interactions that regulate migratory pathways of inflammatory cells in the body and their subsequent activation in the immune recognition process.An array of specialised cell surface structures have been characterised that mediate cell-to-cell and cell-to-matrix contacts, but also exert important signalling functions during cell activation. These cell adhesion molecules are attractive targets for directed immunomodulatory therapies for several reasons. First, such therapies are not dependent on antigen specificity. Secondly, selective regulation of different adhesion molecules allows the possibility of differentiated treatment strategies in different autoimmune conditions.Multiple sclerosis is a neurological disorder characterised by localised infiltrations of primarily T lymphocytes in the CNS. Both T lymphocytes and endothelial cells in the inflammatory lesions associated with the disease express high levels of adhesion molecules. Furthermore, specific blocking of certain adhesion molecules with monoclonal antibodies is an efficient therapy in relevant animal models of multiple sclerosis. These facts make this disorder a candidate for therapies directed against adhesion molecules.