Autoimmune demyelination in the central nervous system.
Autoimmune demyelination was studied in EAE induced by active challenge or by transfer of effector T-cell lines or clones specific for myelin basic protein or proteolipid apoprotein. The following points became clear: (1) Proteolipid apoprotein is responsible for widespread demyelination; (2) demyelination is more significant in EAE with a more chronic disease process; (3) a single T-cell clone can mediate significant demyelination without the aid of recipient-derived T-cell populations; (4) the difference in vulnerability between axons and myelin may account for the T-cell-mediated demyelination; and (5) effector T-cell clones can be activated by allogeneic antigens.
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Division of Demyelinating Disease and Aging, National Institute of Neuroscience, Tokyo, Japan.
D000818:Animals; D001323:Autoantibodies / Q000032:analysis; D001324:Autoantigens / Q000276:immunology; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology* / Q000473:pathology; D008213:Lymphocyte Activation; D051379:Mice; D004676:Myelin Basic Protein / Q000276:immunology*; D009185:Myelin Proteins / Q000276:immunology*; D018991:Myelin Proteolipid Protein; D051381:Rats; D013045:Species Specificity; D013601:T-Lymphocytes / Q000276:immunology*
D001323:Autoantibodies; D001324:Autoantigens; D004676:Myelin Basic Protein; D009185:Myelin Proteins; D018991:Myelin Proteolipid Protein