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  5. Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ
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Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/22447
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dc.contributor.authorMartinez, N. R.en
dc.contributor.authorAugstein, P.en
dc.contributor.authorMoustakas, A. K.en
dc.contributor.authorPapadopoulos, G. K.en
dc.contributor.authorGregori, S.en
dc.contributor.authorAdorini, L.en
dc.contributor.authorJackson, D. C.en
dc.contributor.authorHarrison, L. C.en
dc.date.accessioned2015-11-24T19:24:16Z-
dc.date.available2015-11-24T19:24:16Z-
dc.identifier.issn0021-9738-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/22447-
dc.rightsDefault Licence-
dc.subjectAdministration, Intranasalen
dc.subjectAdoptive Transferen
dc.subjectAnimalsen
dc.subjectCells, Cultureden
dc.subjectDiabetes Mellitus, Type 1/*drug therapy/immunology/metabolismen
dc.subject*Epitopesen
dc.subjectFemaleen
dc.subjectHumansen
dc.subjectMaleen
dc.subjectMiceen
dc.subjectMice, Inbred NODen
dc.subjectModels, Molecularen
dc.subjectPeptides/administration & dosage/*therapeutic useen
dc.subjectProinsulin/chemistry/genetics/metabolism/*therapeutic useen
dc.subjectProtein Bindingen
dc.subjectProtein Structure, Tertiaryen
dc.subjectSpleen/cytology/immunologyen
dc.subjectT-Lymphocytes, Cytotoxic/*immunology/physiologyen
dc.titleDisabling an integral CTL epitope allows suppression of autoimmune diabetes by intranasal proinsulin peptideen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1172/JCI17166-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/12727928-
heal.identifier.secondaryhttp://www.jci.org/articles/view/17166/files/pdf-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2003-
heal.abstractInsulin is a major target of the autoimmune response associated with destruction of pancreatic beta cells in type 1 diabetes. A peptide that spans the junction of the insulin B chain and the connecting (C) peptide in proinsulin has been reported to stimulate T cells from humans at risk for type 1 diabetes and autoimmune diabetes-prone NOD mice. Here we show that proinsulin B24-C36 peptide binds to I-A(g7), the MHC class II molecule of the NOD mouse, and, after intranasal administration, induces regulatory CD4(+) T cells that, in the absence of CD8(+) T cells, block the adoptive transfer of diabetes. Curiously, however, intranasal B24-C36 did not inhibit development of spontaneous diabetes in treated mice. We then determined that B24-C36, and its core sequence B25-C34, bind to K(d), the NOD mouse MHC class I molecule, and elicit CD8(+) CTLs. When the CD8(+) T lymphocyte epitope was truncated at the C34 valine anchor residue for binding to K(d), the residual CD4(+) T cell epitope, B24-C32/33, significantly inhibited diabetes development after a single intranasal dose. This study identifies a novel CTL epitope in proinsulin and demonstrates that the therapeutic potential of a "tolerogenic" autoantigen peptide can be compromised by the presence of an integral CTL epitope.en
heal.journalNameJ Clin Investen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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