Multiple sclerosis is an inflammatory demyelinating disease of the cen
tral nervous system of putative autoimmune origin. In the present revi
ew the hypothesis that autoimmunity against multiple different brain a
ntigens can lead to T-cell mediated brain inflammation and that multip
le different immunological mechanisms may be responsible for the destr
uction of myelin is highlighted. The multitude of possible pathogeneti
c mechanisms is reflected in multiple sclerosis patients by a broad sp
ectrum of disease susceptibility genes and by a profound heterogeneity
of pathology and immunopathogenesis of the lesions.