Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating disease of the central nervous system (CNS). It is regarded as an autoimmune disorder and a complex interplay of genetic and environmental factors governs an individual’s susceptibility to the disease (reviewed in [1]). The initial activation of autoreactive lymphocytes is thought to take place in the systemic lymphoid organs, most likely through molecular mimicry or non-specifically through bystander activation [1]. These autoreactive lymphocytes can migrate to the CNS where they become reactivated upon encountering their target antigen, initiating an autoimmune inflammatory attack. This ultimately leads to demyelination [1].