Multiple sclerosis (MS) is a chronic disabling disease caused by an attack of the immune system on the brain and spinal cord. The cause of the inappropriate immune system activity is still unknown and although the number of therapeutics is increasing, there is still no treatment that can halt or prevent the disease in all patients. The development of new therapies is hindered by the paucity of animal models that accurately reflect the pathogenic mechanism causing MS. The experimental autoimmune encephalomyelitis (EAE) model has been widely used to investigate these pathogenic mechanisms in MS and to test new treatments.

The research of the PhD student Jordon Dunham has been funded via a project from the Marie Skłodowska-Curie research fellowship program of the European Commission (Neurokine). He performed his investigations at the Neuroscience department of the UMCG and at the Biomedical Primate Research Centre (BPRC) in Rijswijk. The research for his thesis had two aims: i) to utilize non-human primate (NHP) models for gaining a better understanding of the pathogenic immune mechanisms underlying MS and ii) to determine how closely NHP models replicate key pathology features of MS.

This thesis describes how a common herpes virus (EBV), which is recognized as an important environmental risk factor of MS, alters the function of B and T lymphocytes and that these changes can have an important role in the pathogenic mechanisms of disease. Another important finding of this thesis was that the pathology in the brain of marmoset monkeys with MS-like disease more closely replicates the brain pathology in MS than the more frequently used rodent models of the disease.

In conclusion, the immunological and pathological proximity of primate EAE models to MS makes them valuable systems for translational research into the role of EBV in the pathogenesis of MS and for the development of innovative treatments.