Pathophysiology of experimental autoimmune encephalomyelitis

Multiple sclerosis (MS) is presumed to be an autoimmune disease of the central nervous system leading to demyelination, axonal damage, and progressive neurologic disability. Although no single animal model can capture all aspects of human MS, the experimental autoimmune encephalomyelitis (EAE) model in rodents immensely improved our understanding of MS pathophysiology. The main advantage of EAE is the genetic engineering of mice to allow researchers to investigate the roles of various genes/molecules in the disease. Data generated from EAE models suggest that disease onset results from an aberrant, T cell-mediated immune response to a number of myelin antigens. We also discuss the importance of other immune cells, such as CD8⁺ T cells, B cells, and macrophages, in the immunopathogenesis of the disease. In summary, the EAE model has helped to elucidate the roles of various cells/molecules in the neuro-inflammatory aspects of MS.