Autoimmune spread to myelin is associated with experimental autoimmune encephalomyelitis induced by a neuronal protein, beta-synuclein.

Accumulating evidence suggests that autoimmunity against neuronal proteins is important for MS pathogenesis. We have characterized T- and B-cell responses associated with experimental autoimmune encephalomyelitis (EAE) induced in Lewis rats with recombinant beta-Synuclein (betaSync), a neuronal component. The encephalitogenic betaSync-specific T cells recognize a single immunodominant region with an epitope delineated at amino acids 97-105; B-cell specificity is more widespread, albeit directed mostly to the C-terminus of betaSync. Most interestingly, betaSync-induced autoimmune T- and B-cell responses spread not only to other neuronal antigens but also to myelin encephalitogens, raising the possibility that anti-neuronal immune attacks could also result in demyelination.