Trimolecular interactions in experimental autoimmune demyelinating disease and prospects for immunotherapy.
Experimental allergic encephalomyelitis (EAE) is a T cell mediated model of demyelinating disease that develops as a result of an autoimmune response to the myelin structural antigen, myelin basic protein (MBP). Much information has accumulated on the nature of trimolecular interactions which lead to the activation of self-reactive T lymphocytes in this disorder. Many parallels exist in the etiopathogenesis of EAE and multiple sclerosis (MS). Based upon these similarities selective immunotherapy that targets either class II molecules of the major histocompatibility complex or T cell receptor variable region genes will be described for EAE with consideration given to application of these principles in MS.
Bell
R B
RB
Department of Neurology, Stanford University School of Medicine, CA 94305-5235.
Steinman
L
L
D000595:Amino Acid Sequence; D000818:Animals; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000209:etiology* / Q000628:therapy; D000939:Epitopes; D006801:Humans; D007167:Immunotherapy; D051379:Mice; D008969:Molecular Sequence Data; D009103:Multiple Sclerosis / Q000235:genetics / Q000276:immunology; D004676:Myelin Basic Protein / Q000737:chemistry / Q000276:immunology; D011948:Receptors, Antigen, T-Cell / Q000235:genetics; D013601:T-Lymphocytes / Q000276:immunology
D000939:Epitopes; D004676:Myelin Basic Protein; D011948:Receptors, Antigen, T-Cell