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dc.contributor.authorOdak, Ivan
dc.contributor.authorDepkat-Jakob, Alina
dc.contributor.authorBeck, Maleen
dc.contributor.authorJarek, Michael
dc.contributor.authorYu, Yan
dc.contributor.authorSeidler, Ursula
dc.contributor.authorDavid, Sascha
dc.contributor.authorGanser, Arnold
dc.contributor.authorFörster, Reinhold
dc.contributor.authorPrinz, Immo
dc.contributor.authorKoenecke, Christian
dc.date.accessioned2020-05-22T12:24:50Z
dc.date.available2020-05-22T12:24:50Z
dc.date.issued2020-04-06
dc.identifier.citationPLoS One. 2020;15(4):e0231222. 2020 Apr 6. doi:10.1371/journal.pone.0231222en_US
dc.identifier.pmid32251446
dc.identifier.doi10.1371/journal.pone.0231222
dc.identifier.urihttp://hdl.handle.net/10033/622266
dc.description.abstracts Metrics Comments Media Coverage Abstract Introduction Material and methods Results Discussion Supporting information Acknowledgments References Reader Comments (0) Media Coverage (0) Figures Abstract IL-17A and IL-17F cytokines are important regulators of acute graft-versus-host-disease (GVHD). However, contrary effects of these cytokines in inflammatory diseases have been reported. To investigate the effects of donor-derived IL-17A and IL-17F on GVHD, we made use of single (Il17a-/- or Il17f-/-) and double deficient (Il17af-/-) allogeneic donor CD4+ T cells. We could demonstrate that transplantation of Il17af-/- CD4+ donor T cells led to aggravated GVHD. However, this phenotype was not observed after transplantation of single, Il17a-/- or Il17f-/-, deficient CD4+ T cells, suggesting redundant effects of IL-17A and IL-17F. Moreover, Il17af-/- cell recipients showed an increase of systemic IFNγ, indicating a heightened pro-inflammatory state, as well as infiltration of IFNγ-secreting CD4+ T cells in the recipients’ intestinal tract. These recipients exhibited significant gut leakage, and markedly macrophage infiltration in the gastrointestinal epithelial layer. Moreover, we saw evidence of impaired recovery of gut epithelial cells in recipients of Il17af-/- CD4+ T cells. In this study, we show that IL-17A/F double deficiency of donor CD4+ T cells leads to accelerated GVHD and therefore highlight the importance of these cytokines. Together, IL-17 cytokines might serve as a brake to an intensified Th1 response, leading to the exacerbated gut damage in acute GVHD.en_US
dc.language.isoenen_US
dc.publisherPLOSen_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleDonor-derived IL-17A and IL-17F deficiency triggers Th1 allo-responses and increases gut leakage during acute GVHD.en_US
dc.typeArticleen_US
dc.identifier.eissn1932-6203
dc.contributor.departmentHZI, Helmholtz Zentrum für Infektionsforschung, GmbH, Inhoffenstr. 7, 38124 Braunschweig, Germany.en_US
dc.identifier.journalPloS oneen_US
dc.source.volume15
dc.source.issue4
dc.source.beginpagee0231222
dc.source.endpage
refterms.dateFOA2020-05-22T12:24:51Z
dc.source.journaltitlePloS one
dc.source.countryUnited States


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