Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7806
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dc.contributor.authorKlebow, Sabrina-
dc.contributor.authorHahn, Matthias-
dc.contributor.authorNikoalev, Alexei-
dc.contributor.authorWunderlich, F. Thomas-
dc.contributor.authorHövelmeyer, Nadine-
dc.contributor.authorKarbach, Susanne-
dc.contributor.authorWaisman, Ari-
dc.date.accessioned2022-10-04T09:27:39Z-
dc.date.available2022-10-04T09:27:39Z-
dc.date.issued2016
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/7821-
dc.description.abstractPsoriasis is an autoimmune skin disease that is associated with aberrant activity of immune cells and keratinocytes. In mice, topical application of TLR7/8 agonist IMQ leads to a skin disorder resembling human psoriasis. Recently, it was shown that the IL-23/ IL-17 axis plays a deciding role in the pathogenesis of human psoriasis, as well as in the mouse model of IMQ-induced psoriasis-like skin disease. A consequence of IL-17A production in the skin includes increased expression and production of IL-6, resulting in the recruitment of neutrophils and other myelomonocytic cells to the site of inflammation. To further investigate and characterize the exact role of IL-6 signaling in myelomonocytic cells during experimental psoriasis, we generated mice lacking the IL-6 receptor alpha specifically in myelomonocytic cells (IL-6RαΔmyel). Surprisingly, disease susceptibility of these mice was not affected in this model. Our study shows that classical IL-6 signaling in myelomonocytic cells does not play an essential role for disease development of IMQ-induced psoriasis-like skin disease.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.titleIL-6 signaling in myelomonocytic cells is not crucial for the development of IMQ-induced psoriasisen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-7806-
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.issue3de
jgu.pages.alternativee0151913de
jgu.publisher.year2016-
jgu.publisher.namePLoSde
jgu.publisher.placeLawrence, Kan.de
jgu.publisher.urihttp://dx.doi.org/10.1371/journal.pone.0151913de
jgu.publisher.issn1932-6203de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
opus.date.modified2018-08-23T08:22:58Z
opus.subject.dfgcode00-000
opus.organisation.stringFB 04: Medizin: II. Medizinische Klinik und Poliklinikde_DE
opus.organisation.stringFB 04: Medizin: Institut für Molekulare Medizinde_DE
opus.identifier.opusid56325
opus.institute.number0426
opus.institute.number0458
opus.metadataonlyfalse
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_EN
opus.affiliatedKarbach, Susanne
opus.affiliatedWaisman, Ari
jgu.publisher.doi10.1371/journal.pone.0151913de
jgu.organisation.rorhttps://ror.org/023b0x485-
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

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