The studies were designed to examine interactions between lymphocytes which induce the model autoimmune disease experimental allergic encephalomyelitis (EAE) and cerebral vascular endothelial (EC) which comprise the blood-brain barrier (BBB). The first part of these experiments examined the capacity of EC to function as targets for lysis by T-cells capable of transferring EAE. Lysis was proportional to E/T ratios, dependent upon the expression of la antigen and the presence of specific antigen. Continuously cultured antigen-specific T-cell lines ultimately lost the ability to lyse EC but continued to proliferate MBP. These cell lines also lost the ability to transfer EAE suggesting a relationship between lytic potential and encephalitogenicity. The second part of these experiments concerned observations that cerebral vascular EC inhibited antigen-induced proliferation by MBP-specific lymphocytes. Attempts to characterize the inhibition indicated that IL-1 induced synthesis of prostacyclin (PGI 2) by EC. The amount of PGI 2 synthesized in these experiments was sufficient to account for the inhibitory response observed. These data indicate that EC-lymphocyte interactions may result in effects on both EC (i.e., lysis) and lymphocytes (i.e., anti-proliferative response). Such interactions may result in alterations of BBB permeability leading to vascular egression into the CNS, which are pathologic hallmarks of neuroimmunological disorders such as EAE and multiple sclerosis.
