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dc.contributor.author Fajka-Boja, Roberta
dc.contributor.author Suhajdáné Urbán, Veronika
dc.contributor.author Szebeni, Gábor
dc.contributor.author Czibula, Ágnes
dc.contributor.author Blaskó, Andrea
dc.contributor.author Kriston-Pál, Éva
dc.contributor.author Makra, Ildikó
dc.contributor.author Hornung, Ákos
dc.contributor.author Szabó, Enikő
dc.contributor.author Than, Nándor Gábor
dc.contributor.author Monostori, Éva
dc.date.accessioned 2016-11-15T09:39:34Z
dc.date.available 2016-11-15T09:39:34Z
dc.date.issued 2016
dc.identifier 84964355522
dc.identifier.citation pagination=360-370; journalVolume=18; journalIssueNumber=3; journalTitle=CYTOTHERAPY;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/3786
dc.identifier.uri doi:10.1016/j.jcyt.2015.12.004
dc.description.abstract BACKGROUND AIMS: Mesenchymal stromal cells (MSCs) have powerful immunosuppressive activity. This function of MSCs is attributed to plethora of the expressed immunosuppressive factors, such as galectin-1 (Gal-1), a pleiotropic lectin with robust anti-inflammatory effect. Nevertheless, whether Gal-1 renders or contributes to the immunosuppressive effect of MSCs has not been clearly established. Therefore, this question was the focus of a complex study. METHODS: MSCs were isolated from bone marrows of wild-type and Gal-1 knockout mice and their in vitro anti-proliferative and apoptosis-inducing effects on activated T cells were examined. The in vivo immunosuppressive activity was tested in murine models of type I diabetes and delayed-type hypersensitivity. RESULTS: Both Gal-1-expressing and -deficient MSCs inhibited T-cell proliferation. Inhibition of T-cell proliferation by MSCs was mediated by nitric oxide but not PD-L1 or Gal-1. In contrast, MSC-derived Gal-1 triggered apoptosis in activated T cells that were directly coupled to MSCs, representing a low proportion of the T-cell population. Furthermore, absence of Gal-1 in MSCs did not affect their in vivo immunosuppressive effect. CONCLUSIONS: These results serve as evidence that Gal-1 does not play a role in the systemic immunosuppressive effect of MSCs. However, a local contribution of Gal-1 to modulation of T-cell response by direct cell-to-cell interaction cannot be excluded. Notably, this study serves a good model to understand how the specificity of a pleiotropic protein depends on the type and localization of the producing effector cell and its target.
dc.relation.ispartof urn:issn:1465-3249
dc.title Galectin-1 is a local but not systemic immunomodulatory factor in mesenchymal stromal cells.
dc.type Journal Article
dc.date.updated 2016-11-14T08:05:05Z
dc.language.rfc3066 en
dc.identifier.mtmt 3024122
dc.identifier.wos 000370914800006
dc.identifier.pubmed 26857229
dc.contributor.department MTA Szegedi Biológiai Kutatóközpont
dc.contributor.department SZTE/DI/Klinikai Orvostudományok Doktori Iskola
dc.contributor.institution MTA Szegedi Biológiai Kutatóközpont
dc.contributor.institution Szegedi Tudományegyetem


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