Immunopathogenic mechanisms in experimental allergic encephalomyelitis

Abstract

Experimental allergic encephalomyelitis, a cell-mediated autoimmune disease, continues to provide interesting data on the mechanisms subserving organ-specific autoimmunity. The elements of the trimolecular complex have been further defined and the conserved molecular basis of the interaction between the T-cell receptor and the major histocompatibility complex class II-peptide antigen complex is better understood. This model also provides new insights into the cellular interactions within the brain during the course of the autoimmune inflammatory response.