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.
Publication types
-
Comparative Study
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Amino Acid Sequence
-
Animals
-
Autoantibodies / biosynthesis
-
Autoantibodies / metabolism*
-
Cell Line
-
Encephalomyelitis, Autoimmune, Experimental / chemically induced
-
Encephalomyelitis, Autoimmune, Experimental / genetics
-
Encephalomyelitis, Autoimmune, Experimental / immunology*
-
Epitopes, T-Lymphocyte / immunology
-
Epitopes, T-Lymphocyte / metabolism
-
Female
-
Humans
-
Mice
-
Molecular Sequence Data
-
Myelin Sheath / immunology*
-
Myelin Sheath / metabolism*
-
Rats
-
Rats, Inbred Lew
-
Recombinant Proteins / administration & dosage
-
Recombinant Proteins / toxicity
-
beta-Synuclein / physiology*
-
beta-Synuclein / toxicity
Substances
-
Autoantibodies
-
Epitopes, T-Lymphocyte
-
Recombinant Proteins
-
SNCB protein, human
-
Sncb protein, mouse
-
beta-Synuclein