Although lymphocyte traffic through the brain is normally low, this can increase dramatically in response to infection or an autoimmune reaction. We have studied the adhesion of lymphocytes to cerebral endothelium in vitro in an attempt to model the first step of the infiltration process--that is, the initial interaction between the lymphocytes and endothelial cells--by brief co-culture of lymph node cells with monolayers of cultured cerebral endothelium. In this system we find that the basal level of adhesion can be increased in a dose-dependent manner by pre-treatment of the endothelial cells with interferon-gamma (IFN-gamma) and/or tumour necrosis factor (TNF) but not with interleukin-1 (IL-1). This increased adhesion can be blocked by incubating the IFN-gamma-treated cells with an antibody that is thought to bind to the common beta-chain of the lymphocyte functional antigen-1 (LFA-1) family of molecules. This suggests that endothelial cells express either LFA-1 or a molecule sharing the beta-subunit (of which several have been described) and furthermore that this molecule is involved in the regulation of lymphocyte traffic into the brain.