EAE induced with MOG peptide (35-55) in C57BL/6 mice are the most frequently used model and is a reliable, reproducible and well characterized model. The immunogenic epitope MOG35-55 is emulsified in CFA and injected s.c. followed by two pertussis toxin injections i.p. (d0 and day 2). Mice develop a monophasic EAE with ascending flaccid paralysis around 1-2 weeks after immunization. Myelin-specific T cells are activated in the periphery and migrate into the CNS across the blood-brain-barrier. Upon entry into the CNS, T cells are re-activated by antigen-presenting cells, ultimately resulting in demyelination and axonal cell death. Pertussis toxin has been suggested to modulate the blood-brain barrier.
MOG35-55 induced EAE is a severe monophasic, demyelinating encephalomyelitis with onset after around 1-2 weeks and reaches maximum score a few days later.
In this model, disease is accompanied by demyelination of the CNS, which can be assessed by histology at termination. In addition, recall IL-17 and IFN-g responses from LNs cells can be assayed ex vivo either as a measurement of drug efficacy or prediction of efficacy for selection of lead compounds before in vivo experiment.