Autoimmune spread to myelin is associated with experimental autoimmune encephalomyelitis induced by a neuronal protein, β-Synuclein

Neta Kela-Madar, Nicole Kerlero de Rosbo, Ayal Ronen, Felix Mor, Avraham Ben-Nun*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

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 β-Synuclein (βSync), a neuronal component. The encephalitogenic βSync-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 βSync. Most interestingly, βSync-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.

Original languageEnglish
Pages (from-to)19-29
Number of pages11
JournalJournal of Neuroimmunology
Volume208
Issue number1-2
DOIs
StatePublished - 31 Mar 2009
Externally publishedYes

Funding

FundersFunder number
William Sahm Foundation
National Multiple Sclerosis Society
Israel Science Foundation
Ministry of Health, State of Israel

    Keywords

    • Antigens/peptides/epitopes
    • Autoantibodies
    • Autoimmunity
    • Rodent
    • T cells

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