ABSTRACT
Several lines of evidence suggest that a sequence of environmental triggers upset the delicate balance between tolerance and nontolerance of ‘‘self’’ antigens, but the environmental triggers and the detailed immunogenetic predisposing factors are unknown. Though the exact etiopathogenesis of multiple sclerosis (MS) is unknown, the leading theory suggests that T-cells are the conductors of a misdirected immune response that targets myelin in the central nervous system (CNS). They recruit many other components of the innate and adaptive immune system, producing the inflammation seen pathologically in the CNS (1,2). Subsequently, epitope spreading and immunological memory develop and give rise to the chronicity of the disease.
