Abstract
IntroductionMultiple sclerosis (MS) is an enigmatic autoimmune-driven inflammatory/demyelinating disease of the human central nervous system (CNS), affecting brain, spinal cord, and optic nerves. The cause of the disease is not known and the number of effective treatments is limited. Despite some clear successes, translation of immunological discoveries in the mouse experimental autoimmune encephalomyelitis (EAE) model into effective therapies for MS patients has been difficult. This translation gap between MS and its elected EAE animal model reflects the phylogenetic distance between humans and their experimental counterpart, the inbred/specific pathogen free (SPF) laboratory mouse.ObjectiveHere, we discuss that important new insights can be obtained into the mechanistic basis of the therapy paradox from the study of nonhuman primate EAE (NHP-EAE) models, the well-validated EAE model in common marmosets (Callithrix jacchus) in particular.InterpretationData presented in this review demonstrate that due to a considerable immunological and pathological overlap with mouse EAE on one side and MS on the other, the NHP EAE model can help us bridge the translation gap.
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