[Inflammatory mechanisms in nervous system].

Experimental autoimmune encephalomyelitis (EAE), is a neuroautoimmune inflammatory disease, involving sensitization to central nervous system myelin basic protein (MBP). Our studies of the coagulation system and ensuing fibrinolysis implicate coagulation and cleavage of fibrin within or on the luminal surface of the cerebrovasculature, as events initiating the inflammation characterizing EAE. Among recipient rats injected with MBP-primed, cultured-activated lymph node cells, "opening" the blood-brain barrier (BBB) and deposition of perivascular fibrin within the spinal cord occur in parallel one day before onset of clinical signs of EAE. The critical event precipitating EAE is a binding of circulating MBP-reactive immune effector cells to MBP immunodeterminants on the surface of cerebrovascular endothelial cells. Coagulation and ensuring fibrinolysis occur at sites of binding of effector cells to cerebrovascular endothelium. Release of biologically active peptides, cleaved from fibrin, "open" the BBB. Once BBB is opened, even transiently, the stage is set for a complex cascade of immunologically-nonspecific inflammatory events, which plays an important role in the development of tissue damage, including demyelination.