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*
Department of Immunobiology, Biomedical Primate Research Centre, Rijswijk, The Netherlands;
Department of Neurological Science, University of Genova, Genova, Italy;
Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel;
§
Department of Immunology, Erasmus University of Rotterdam, Rotterdam, The Netherlands; and
¶
Department of Experimental In Vivo NMR, Image Sciences Institute, Utrecht University, Utrecht, The Netherlands
Immunization of common marmosets (Callithrix jacchus) with a single dose of human myelin in CFA, without administration of Bordetella pertussis, induces a form of autoimmune encephalomyelitis (EAE) resembling in its clinical and pathological expression multiple sclerosis in humans. The EAE incidence in our outbred marmoset colony is 100%. This study was undertaken to assess the genetic and immunological basis of the high EAE susceptibility. To this end, we determined the separate contributions of immune reactions to myelin/oligodendrocyte glycoprotein (MOG) and myelin basic protein to the EAE induction. Essentially all pathological features of myelin-induced EAE were also found in animals immunized with MOG in CFA, whereas in animals immunized with myelin basic protein in CFA clinical and pathological signs of EAE were lacking. The epitope recognition by anti-MOG Abs and T cells were assessed. Evidence is provided that the initiation of EAE is based on T and B cell activation by the encephalitogenic phMOG14–36 peptide in the context of monomorphic Caja-DRB*W1201 molecules.
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