Fast Progression of Recombinant Human Myelin/Oligodendrocyte Glycoprotein (MOG)-Induced Experimental Autoimmune Encephalomyelitis in Marmosets Is Associated with the Activation of MOG34–56-Specific Cytotoxic T Cells

摘要: The recombinant human (rh) myelin/oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) model in the common marmoset is characterized by 100% disease incidence, a chronic course, and variable time interval between immunization neurological impairment. We investigated whether monkeys with fast slow progression display different anti-MOG T or B cell responses analyzed underlying pathogenic mechanism(s). results show that progressor significantly wider specificity diversification of cells at necropsy than progressors, especially against MOG(34-56) MOG(74-96). emerged as critical encephalitogenic peptide, inducing severe multiple lesions inflammation, demyelination, axonal injury CNS. Although EAE was not observed MOG(74-96)-immunized monkeys, weak low grade CNS pathology were detected. When these cases received booster IFA, full-blown developed. MOG(34-56)-reactive expressed CD3, CD4, CD8 CD56, but CD16. Moreover, MOG(34-56)-specific lines displayed specific cytotoxic activity peptide-pulsed lines. phenotype suggest are NK-CTL. These support concept may play role pathogenesis sclerosis.