Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7766
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dc.contributor.authorMufazalov, Ilgiz A.-
dc.contributor.authorRegen, Tommy-
dc.contributor.authorSchelmbauer, Carsten-
dc.contributor.authorKuschmann, Janina-
dc.contributor.authorMuratova, Alisa M.-
dc.contributor.authorNikolaev, Alexei-
dc.contributor.authorMüller, Werner-
dc.contributor.authorPinteaux, Emmanuel-
dc.contributor.authorWaisman, Ari-
dc.date.accessioned2022-09-15T07:32:33Z-
dc.date.available2022-09-15T07:32:33Z-
dc.date.issued2016
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/7781-
dc.description.abstractInterleukin-1 (IL-1) plays a crucial role in numerous inflammatory diseases via action on its only known signaling IL-1 receptor type 1 (IL-1R1). To investigate the role of IL-1 signaling in selected cell types, we generated a new mouse strain in which exon 5 of the Il1r1 gene is flanked by loxP sites. Crossing of these mice with CD4-Cre transgenic mice resulted in IL-1R1 loss of function specifically in T cells. These mice, termed IL-1R1ΔT, displayed normal development under steady state conditions. Importantly, isolated CD4 positive T cells retained their capacity to differentiate toward Th1 or Th17 cell lineages in vitro, and strongly proliferated in cultures supplemented with either anti-CD3/CD28 or Concanavalin A, but, as predicted, were completely unresponsive to IL-1β administration. Furthermore, IL-1R1ΔT mice were protected from gut inflammation in the anti-CD3 treatment model, due to dramatically reduced frequencies and absolute numbers of IL-17A and interferon (IFN)-γ producing cells. Taken together, our data shows the necessity of intact IL-1 signaling for survival and expansion of CD4 T cells that were developed in an otherwise IL-1 sufficient environment.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizinde
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleGeneration of a novel T cell specific interleukin-1 receptor type 1 conditional knock out mouse reveals intrinsic defects in survival, expansion and cytokine production of CD4 T cellsen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-7766-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titlePLoS onede
jgu.journal.volume11de
jgu.journal.issue8de
jgu.pages.alternativee0161505de
jgu.publisher.year2016-
jgu.publisher.namePLoSde
jgu.publisher.placeLawrence, Kan.de
jgu.publisher.urihttp://dx.doi.org/10.1371/journal.pone.0161505de
jgu.publisher.issn1932-6203de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
opus.date.modified2018-08-23T08:50:45Z
opus.subject.dfgcode00-000
opus.organisation.stringFB 04: Medizin: Institut für Physiologische Chemie und Pathobiochemiede_DE
opus.organisation.stringFB 04: Medizin: Institut für Molekulare Medizinde_DE
opus.identifier.opusid56403
opus.institute.number0404
opus.institute.number0458
opus.metadataonlyfalse
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_EN
opus.affiliatedMufazalov, Ilgiz A.
opus.affiliatedWaisman, Ari
jgu.publisher.doi10.1371/journal.pone.0161505de
jgu.organisation.rorhttps://ror.org/023b0x485-
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

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