Using the well-validated experimental autoimmune encephalomyelitis (EAE) model in common marmosets (Callithrix jacchus), a small bodied Neotropical primate, we have explored how pathogenic T cells specific for the pathogenically relevant myelin antigen myelin oligodendrocyte glycoprotein (MOG) (Jagessar et al. 2008) are maintained inactive in healthy animals and how they are activated under conditions relevant to multiple sclerosis (MS), the human disease on which the EAE model has been projected. The gene discussed is MOG; the disease is multiple sclerosis.