Cell surface endothelial proteins altered in experimental allergic encephalomyelitis.

Endothelial cells (EC) are increasingly being considered as important participants in the early evolution of inflammatory and immune responses in experimental allergic encephalomyelitis (EAE). We have found that a mouse monoclonal antibody, which reacts with the luminal plasma membrane of central nervous system endothelium, detects an alteration in the blood-brain barrier (BBB) in lesions in Lewis rats with EAE. Anti-endothelial barrier antigen (EBA) reacted with microvessels in normal rat brain and spinal cord. This reaction was abolished in 'EAE' microvessels surrounded by inflammatory cells. In rats that had recovered from one attack most EC reacted with the antibody, indicating that EBA was reexpressed during recovery. However, blood vessels in areas with residual inflammatory lesions were negative. The biochemical changes that lead to this absence of antibody binding and the cells or mediators responsible for producing this change are not yet known. However, anti-EBA should provide a useful tool for exploring molecular mechanisms underlying BBB breakdown.