Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/18496
Full metadata record
DC FieldValueLanguage
dc.contributor.authorZou, L. P.en
dc.contributor.authorDeretzi, G.en
dc.contributor.authorPelidou, S. H.en
dc.contributor.authorLevi, M.en
dc.contributor.authorWahren, B.en
dc.contributor.authorQuiding, C.en
dc.contributor.authorvan der Meide, P.en
dc.contributor.authorZhu, J.en
dc.date.accessioned2015-11-24T18:53:06Z-
dc.date.available2015-11-24T18:53:06Z-
dc.identifier.issn0028-3908-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/18496-
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subjectImmunoglobulin G/analysisen
dc.subjectImmunohistochemistryen
dc.subjectMaleen
dc.subjectNeuritis, Autoimmune, Experimental/*drug therapy/immunology/metabolismen
dc.subjectPeptides/immunologyen
dc.subjectPhosphodiesterase Inhibitors/administration & dosage/*therapeutic useen
dc.subjectRatsen
dc.subjectRats, Inbred Lewen
dc.subjectRecurrence/prevention & controlen
dc.subjectRolipram/administration & dosage/*therapeutic useen
dc.subjectT-Lymphocytes/drug effects/physiologyen
dc.subjectTumor Necrosis Factor-alpha/metabolismen
dc.titleRolipram suppresses experimental autoimmune neuritis and prevents relapses in Lewis ratsen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/10670428-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2000-
heal.abstractRolipram, a phosphodiesterase type 4 inhibitor, can markedly down-regulate antigen-driven T cell proliferation and suppress TNF-alpha production in vitro and in vivo. Here we report the effects of Rolipram on experimental autoimmune neuritis (EAN), which can be induced by immunization with myelin components of the peripheral nervous system (PNS) combined with Freund's complete adjuvant (FCA), and which represents a CD4+ T cell-mediated animal model for human Guillain-Barre syndrome. EAN induced in Lewis rats by inoculation with the PNS P2 protein peptide 57-81 and FCA was strongly suppressed by Rolipram administered twice daily intraperitoneally from day 9 post immunization (p.i.), i.e. after onset of clinical EAN. Suppression of EAN was associated with down-regulated myelin antigen-induced T cell responses as well as down-regulated IFN-gamma and TNF-alpha production. A relapse of clinical EAN occurred upon treatment of a short duration (7 days), while prolongation of treatment resulted in the prevention of clinical EAN relapse. There was no relationship between clinical EAN relapse and high levels of TNF-alpha. The immunomodulatory effects of Rolipram call for further research into the potential role of drugs acting on the immune system in the treatment of autoimmune diseases.en
heal.journalNameNeuropharmacologyen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

Files in This Item:
There are no files associated with this item.


This item is licensed under a Creative Commons License Creative Commons