{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T01:22:20Z","timestamp":1789435340386,"version":"build-2803163510"},"reference-count":29,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2017,3,8]],"date-time":"2017-03-08T00:00:00Z","timestamp":1488931200000},"content-version":"vor","delay-in-days":7,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100008392","name":"Sundhed og Sygdom, Det Frie Forskningsr\u00e5d","doi-asserted-by":"publisher","award":["4092\u201000024B"],"award-info":[{"award-number":["4092\u201000024B"]}],"id":[{"id":"10.13039\/100008392","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100004336","name":"Novartis","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004336","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100006286","name":"Kongelig Hofbuntmager Aage Bangs Fond","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100006286","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2017,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Psoriasis is a common chronic inflammatory and immune\u2010mediated skin disease. Antagonists of <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1 and, recently, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 have proven to be highly effective in the treatment for psoriasis; however, the molecular mechanisms involved in the pathogenesis of psoriasis are poorly understood. Recently, we presented evidence that I\u03baB\u03b6 is a key regulator in the development of psoriasis through its role in mediating <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A\u2010driven effects. Like <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017F is produced by a variety of immune cells, and the expression of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017F is increased in psoriatic skin. The purpose of this study was to characterize the role of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017F in the regulation of I\u03baB\u03b6 expression and to investigate whether <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017F regulates psoriasis\u2010associated genes in human keratinocytes through I\u03baB\u03b6. Here, we demonstrate that <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017F stimulation induces I\u03baB\u03b6 expression at both the <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> and the protein levels in normal human keratinocytes. Moreover, silencing I\u03baB\u03b6 by si<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> revealed that I\u03baB\u03b6 is a key regulator of specific <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017F\u2010inducible psoriasis\u2010associated genes and proteins, including <jats:styled-content style=\"fixed-case\">DEFB<\/jats:styled-content>4\/hBD2, S100A7, <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>20, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108 and <jats:styled-content style=\"fixed-case\">CHI<\/jats:styled-content>3L1. In addition, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017F\u2010induced I\u03baB\u03b6 expression is mediated by a mechanism involving the p38 <jats:styled-content style=\"fixed-case\">MAPK<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03baB signalling pathways, as shown by the clear reduction in <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017F\u2010mediated expression of I\u03baB\u03b6 during chemical inhibition of these two signalling pathways. In summary, we present I\u03baB\u03b6 as a novel key regulator of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017F\u2010driven effects in psoriasis. Thus, antagonists to I\u03baB\u03b6 could potentially provide a more targeted approach for treating psoriasis as well as for treating the other inflammatory and immune\u2010mediated diseases for which <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017\u2010targeting drugs have recently been approved.<\/jats:p>","DOI":"10.1111\/exd.13182","type":"journal-article","created":{"date-parts":[[2016,8,30]],"date-time":"2016-08-30T13:35:49Z","timestamp":1472564149000},"page":"234-241","source":"Crossref","is-referenced-by-count":36,"title":["<scp>IL<\/scp>\u201017F regulates psoriasis\u2010associated genes through I\u03baB\u03b6"],"prefix":"10.1111","volume":"26","author":[{"given":"Trine","family":"Bertelsen","sequence":"first","affiliation":[{"name":"Department of Dermatology Aarhus University Hospital  Aarhus C Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christine","family":"Ljungberg","sequence":"additional","affiliation":[{"name":"Department of Dermatology Aarhus University Hospital  Aarhus C Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rasmus","family":"Boye Kjellerup","sequence":"additional","affiliation":[{"name":"Department of Dermatology Aarhus University Hospital  Aarhus C Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lars","family":"Iversen","sequence":"additional","affiliation":[{"name":"Department of Dermatology Aarhus University Hospital  Aarhus C Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claus","family":"Johansen","sequence":"additional","affiliation":[{"name":"Department of Dermatology Aarhus University Hospital  Aarhus C 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