Abstract
Our studies have focused on the mechanisms involved in blood-brain barrier and blood-nerve barrier alterations in inflammatory demyelinating diseases. The results support the conclusion that these diseases are initiated by delayed hypersensitivity reactions. They further demonstrate a role for mast cell degranulation and vasoactive amines in the peripheral nerve. In the central nervous system, our studies have documented both active and passive mechanisms of edema formation and support the conclusion that cytokines may be involved in altered blood-brain barrier permeability and inflammation. We conclude that several mechanisms of barrier breakdown are activated in the inflammatory demyelinating diseases and that alteration in endothelial cell function is a major component of disease induction.
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