Abstract
Experimental autoimmune neuritis (EAN) is an autoimmune inflammatory demyelinating disease of the peripheral nervous system (PNS), and represents an animal model of the human Guillain–Barré syndrome (GBS). In this study, we report that nasal administration of the neuritogenic peptide 180–199 and of the cryptic peptide 56–71 of the rat neuritogenic P0 protein of peripheral nerve myelin prevents EAN and attenuates ongoing EAN. Both peptides effectively decreased the severity and shortened clinical EAN. Both a prophylactic and a therapeutic approach proved to be beneficial. These effects were associated with T and B cells hyporesponsiveness to the peptide antigens, reflected by downregulated Th1 cell responses (interferon-γ secretion) and macrophage function, whereas Th2 cell responses (IL-4 secretion) and transforming growth factor-β mRNA expression were upregulated.
Published Version
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