Rhesus monkeys immunized with MOG34-56, a dominant T-cell epitope from myelin/oligodendrocyte glycoprotein, develop an acute neurological disease resembling acute disseminated encephalomyelitis (ADEM) in humans. The typical large demyelinated lesions and mononuclear infiltrates in the monkey brains are caused by MOG34-56T-cells. We show that MOG34-56-reactive CD4+ and CD8+ T-cells are induced in monkeys immunized with a peptide from the human CMV major capsid protein (UL86; 981-1003), that shares sequence similarity with MOG34-56. Monkeys sensitized against the viral peptide and subsequently challenged with MOG34-56display histological signs of encephalitis, but do not show overt neurological signs.

ADEM, Autoimmunity, CMV, EAE, MS, Primate
dx.doi.org/10.1016/j.jneuroim.2006.10.010, hdl.handle.net/1765/35869
Journal of Neuroimmunology
Erasmus MC: University Medical Center Rotterdam

Brok, H.P.M, Boven, L.A, van Meurs, M, Kerlero de Rosbo, N, Celebi-Paul, L, Kap, Y.S, … 't Hart, B.A. (2007). The human CMV-UL86 peptide 981-1003 shares a crossreactive T-cell epitope with the encephalitogenic MOG peptide 34-56, but lacks the capacity to induce EAE in rhesus monkeys. Journal of Neuroimmunology, 182(1-2), 135–152. doi:10.1016/j.jneuroim.2006.10.010