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dc.date.accessioned2020-09-16T18:17:10Z
dc.date.available2020-09-16T18:17:10Z
dc.date.created2020-04-15T12:08:36Z
dc.date.issued2020
dc.identifier.citationPietka, Wojciech Sundnes, Olav Hammarström, Clara Louise Zucknick, Manuela Khnykin, Denis Haraldsen, Guttorm . Lack of interleukin-33 and its receptor does not prevent calcipotriol-induced atopic dermatitis-like inflammation in mice. Scientific Reports. 2020, 10:6451, 1-8
dc.identifier.urihttp://hdl.handle.net/10852/79451
dc.description.abstractCurrent studies addressing the influence of interleukin-33 or its receptor (IL-33R/ST2) on development of atopic dermatitis-like inflammation in mice have reported conflicting results. We compared the response in single- and double-deficient IL-33−/−/ST2−/− C57BL/6J BomTac mice in the well-established calcipotriol-induced model of atopic dermatitis. All genotypes (groups of up to 14 mice) developed atopic dermatitis-like inflammation yet we observed no biologically relevant difference between groups in gross anatomy or ear thickness. Moreover, histological examination of skin revealed no differences in mononuclear leukocyte and granulocyte infiltration nor Th2 cytokine levels (IL-4 and IL-13). Finally, skin CD45+ cells and CD3+ cells were found at similar densities across all groups. Our findings indicate that lack of interleukin-33 and its receptor ST2 does not prevent the development of AD-like skin inflammation.
dc.languageEN
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleLack of interleukin-33 and its receptor does not prevent calcipotriol-induced atopic dermatitis-like inflammation in mice
dc.typeJournal article
dc.creator.authorPietka, Wojciech
dc.creator.authorSundnes, Olav
dc.creator.authorHammarström, Clara Louise
dc.creator.authorZucknick, Manuela
dc.creator.authorKhnykin, Denis
dc.creator.authorHaraldsen, Guttorm
cristin.unitcode185,53,18,13
cristin.unitnameAvdeling for patologi
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.cristin1806323
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Scientific Reports&rft.volume=10:6451&rft.spage=1&rft.date=2020
dc.identifier.jtitleScientific Reports
dc.identifier.volume10
dc.identifier.issue1
dc.identifier.doihttps://doi.org/10.1038/s41598-020-63410-z
dc.identifier.urnURN:NBN:no-82566
dc.type.documentTidsskriftartikkel
dc.type.peerreviewedPeer reviewed
dc.source.issn2045-2322
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/79451/2/Pietka_Sci%2BRep_postnr%2B1806323.pdf
dc.type.versionPublishedVersion
cristin.articleid6451


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