1. Autoimmune spread to myelin is associated with experimental autoimmune encephalomyelitis induced by a neuronal protein, β-Synuclein
- Author
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Avraham Ben-Nun, Ayal Ronen, Nicole Kerlero de Rosbo, Neta Kela-Madar, and Felix Mor
- Subjects
Encephalomyelitis, Autoimmune, Experimental ,Encephalomyelitis ,Molecular Sequence Data ,Immunology ,Epitopes, T-Lymphocyte ,medicine.disease_cause ,Epitope ,Cell Line ,Autoimmunity ,Myelin oligodendrocyte glycoprotein ,Mice ,Myelin ,beta-Synuclein ,medicine ,Animals ,Humans ,Immunology and Allergy ,Amino Acid Sequence ,Myelin Sheath ,Autoantibodies ,biology ,Experimental autoimmune encephalomyelitis ,Autoantibody ,medicine.disease ,Recombinant Proteins ,Rats ,Myelin basic protein ,medicine.anatomical_structure ,nervous system ,Neurology ,Rats, Inbred Lew ,biology.protein ,Female ,Neurology (clinical) - Abstract
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.
- Published
- 2009