Crucial role of granulocytic myeloid-derived suppressor cells in the regulation of central nervous system autoimmune disease

dc.contributor.authorIoannou, M.en
dc.contributor.authorAlissafi, T.en
dc.contributor.authorLazaridis, I.en
dc.contributor.authorDeraos, G.en
dc.contributor.authorMatsoukas, J.en
dc.contributor.authorGravanis, A.en
dc.contributor.authorMastorodemos, V.en
dc.contributor.authorPlaitakis, A.en
dc.contributor.authorSharpe, A.en
dc.contributor.authorBoumpas, D. T.en
dc.contributor.authorVerginis, P.en
dc.date.accessioned2015-11-24T19:26:12Z
dc.date.available2015-11-24T19:26:12Z
dc.identifier.issn1550-6606-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/22703
dc.rightsDefault Licence-
dc.titleCrucial role of granulocytic myeloid-derived suppressor cells in the regulation of central nervous system autoimmune diseaseen
heal.abstractThere is a need in autoimmune diseases to uncover the mechanisms involved in the natural resolution of inflammation. In this article, we demonstrate that granulocytic myeloid-derived suppressor cells (G-MDSCs) abundantly accumulate within the peripheral lymphoid compartments and target organs of mice with experimental autoimmune encephalomyelitis prior to disease remission. In vivo transfer of G-MDSCs ameliorated experimental autoimmune encephalomyelitis, significantly decreased demyelination, and delayed disease onset through inhibition of encephalitogenic Th1 and Th17 immune responses. Exposure of G-MDSCs to the autoimmune milieu led to up-regulation of the programmed death 1 ligand that was required for the G-MDSC-mediated suppressive function both in vitro and in vivo. Importantly, myeloid-derived suppressor cells were enriched in the periphery of subjects with active multiple sclerosis and suppressed the activation and proliferation of autologous CD4(+) T cells ex vivo. Collectively, this study revealed a pivotal role for myeloid-derived suppressor cells in the regulation of multiple sclerosis, which could be exploited for therapeutic purposes.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.primary10.4049/jimmunol.1101816-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/22210912-
heal.identifier.secondaryhttp://www.jimmunol.org/content/188/3/1136-
heal.journalNameJ Immunolen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2012-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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