Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system of putative autoimmune origin. In the present review the hypothesis that autoimmunity against multiple different brain antigens can lead to T-cell mediated brain inflammation and that multiple different immunological mechanisms may be responsible for the destruction of myelin is highlighted. The multitude of possible pathogenetic mechanisms is reflected in multiple sclerosis patients by a broad spectrum of disease susceptibility genes and by a profound heterogeneity of pathology and immunopathogenesis of the lesions.