Chapter 4 Immunology of Multiple Sclerosis

Abstract

Publisher Summary This chapter describes the immunology of multiple sclerosis (MS). MS is the most common inflammatory demyelinating disease of the central nervous system (CNS) in young adults. Current knowledge indicates that tissue damage in MS is due to a T-cell-mediated autoimmune process, although antibodies and vulnerability of myelin, oligodendrocytes, and axons also contribute to the heterogeneous phenotypes of MS. MS develops in susceptible individuals, and both a complex predisposing genetic trait and environmental triggers are involved in disease initiation. Once MS has been triggered, a pathogenic autoimmune T-cell response directed against myelin/CNS components perpetuates the disease, although other factors are also involved. MS affects mostly young and middle-aged adults, with the highest prevalence in Northern Europe and North America. Over its protracted course it leads to substantial disability in more than half of patients. The etiology of MS remains unclear; however, the histological picture of MS lesions, genetic data, and the parallels to experimental allergic/autoimmune encephalomyelitis (EAE) and to the response to immunomodulation or suppression all support the concept that MS is an autoimmune disease that is mediated by aberrantly activated CD4+ T helper cells with specificity for myelin components.