P0 glycoprotein peptides 56-71 and 180-199 dose-dependently induce acute and chronic experimental autoimmune neuritis in Lewis rats associated with epitope spreading

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dc.contributor.authorZhu, J.en
dc.contributor.authorPelidou, S. H.en
dc.contributor.authorDeretzi, G.en
dc.contributor.authorLevi, M.en
dc.contributor.authorMix, E.en
dc.contributor.authorvan der Meide, P.en
dc.contributor.authorWinblad, B.en
dc.contributor.authorZou, L. P.en
dc.date.accessioned2015-11-24T19:00:21Z
dc.date.available2015-11-24T19:00:21Z
dc.identifier.issn0165-5728-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/19515
dc.rightsDefault Licence-
dc.subjectAcute Diseaseen
dc.subjectAmino Acid Sequenceen
dc.subjectAnimalsen
dc.subjectB-Lymphocytes/immunologyen
dc.subjectChronic Diseaseen
dc.subjectDisease Models, Animalen
dc.subjectDose-Response Relationship, Immunologicen
dc.subjectEncephalomyelitis, Autoimmune, Experimental/chemically induced/*immunologyen
dc.subjectGuillain-Barre Syndrome/immunologyen
dc.subjectImmunodominant Epitopes/*immunologyen
dc.subjectInterferon-gamma/immunology/secretionen
dc.subjectMaleen
dc.subjectMolecular Sequence Dataen
dc.subjectMyelin P0 Protein/chemistry/*immunology/*pharmacologyen
dc.subjectPeptide Fragments/immunology/pharmacologyen
dc.subjectRatsen
dc.subjectRats, Inbred Lewen
dc.titleP0 glycoprotein peptides 56-71 and 180-199 dose-dependently induce acute and chronic experimental autoimmune neuritis in Lewis rats associated with epitope spreadingen
heal.abstractTwo synthetic peripheral nerve myelin P0 protein peptides, an immunodominant (amino acids 180-199) and a cryptic (amino acids 56-71) one, induced an acute or chronic course of experimental autoimmune neuritis (EAN) in Lewis rats, when given at low dose (50-100 microg/rat) or high dose (250 microg/rat), respectively. Corresponding to the different clinical course, pathological changes and immune responses were found: (1) Onset of clinical signs of P0 peptide 56-71 (P0 56-71) induced EAN was 1-3 days later than in P0 peptide 180-199 (P0 180-199) induced EAN at all immunizing doses, whereas the peak of the disease occurred at a similar time point post immunization (p.i.), i.e. at days 14-16 p.i. in P0 56-71 induced EAN and at day 16 p.i. in P0 180-199 induced EAN. (2) Intramolecular epitope spreading as assessed by delayed type hypersensitivity response occurred in P0 56-71 induced EAN at both low and high antigen doses and in P0 180-199 induced EAN at high antigen dose (250 microg/rat) only. (3) P0 180-199 stimulated higher levels of interferon-gamma production in P0 180-199 induced EAN than in P0 56-71 induced EAN and vice versa. (4) Histopathologic evaluation revealed a similar grade of mononuclear cell infiltration in the sciatic nerves of both types of EAN, but more severe demyelination was found in P0 180-199 induced EAN compared to P0 56-71 induced EAN. The results support the hypothesis that high dose autoantigen immunization induces extensive determinant spreading and chronic course of autoimmune diseases.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/11240020-
heal.journalNameJ Neuroimmunolen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2001-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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