ABSTRACT
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) characterized by demyelination, focal infiltration of inflammatory cells and axonal injury, which leads to loss of neurological function. The exact cause of the disease remains unclear, but an autoimmune response directed against CNS antigens is suspected. Studies in experimental autoimmune encephalomyelitis (EAE), an animal model of MS, have provided important insights into mechanisms of T cell-mediated CNS autoimmune disease. It appears likely that when a genetically susceptible host encounters a common environmental antigen (such as an infectious organism), a process called 'molecular mimicry' results in the peripheral activation of cross-reactive T cells that can migrate to the CNS and mount pro-inflammatory responses to myelin epitopes. This review describes the current understanding on the immunopathogenesis of MS and the mechanisms of action of currently available disease-modifying therapies in the context of the underlying immunopathogenic processes they are thought to affect.