Augmentation of demyelination in rat acute allergic encephalomyelitis by circulating mouse monoclonal antibodies directed against a myelin/oligodendrocyte glycoprotein.
In this study the authors have developed a model with which can be studied directly the influence of circulating anti-myelin antibody on the clinical and pathologic course of inflammatory T-cell-mediated experimental allergic encephalomyelitis (EAE) in the rat. EAE was induced by passive transfer of either myelin basic protein (MBP)-activated spleen cells derived from sensitized donors or long-term-cultured MBP-specific T-cell lines. At the onset of the disease, monoclonal antibodies against a myelin/oligodendrocyte glycoprotein (MOG) were injected intravenously. This antigen is exposed on the surface of central nervous system myelin and oligodendrocytes. Intravenous injection of the antibody in the course of T-cell-mediated transfer EAE augmented the severity and duration of clinical signs and resulted in the formation of large, confluent demyelinated plaques.
D000818:Animals; D000911:Antibodies, Monoclonal / Q000009:adverse effects; D003711:Demyelinating Diseases / Q000209:etiology*; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000150:complications*; D004797:Enzyme-Linked Immunosorbent Assay; D006207:Half-Life; D007150:Immunohistochemistry; D051379:Mice; D008854:Microscopy, Electron; D009185:Myelin Proteins / Q000276:immunology*; D018992:Myelin-Associated Glycoprotein; D051381:Rats; D011917:Rats, Inbred Lew
D000911:Antibodies, Monoclonal; D009185:Myelin Proteins; D018992:Myelin-Associated Glycoprotein