{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T11:49:54Z","timestamp":1789386594567,"version":"build-2803163510"},"reference-count":38,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[1999,3,1]],"date-time":"1999-03-01T00:00:00Z","timestamp":920246400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001300","name":"Foundation for Skin Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001300","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100013126","name":"Psoriasis Association","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100013126","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000848","name":"University of Edinburgh","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000848","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[1999,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Psoriasis is a chronic inflammatory dermatosis characterized by hyperproliferative keratinocytes (KC). The skin lesions are infiltrated by T cells, which secrete gamma interferon (\u03b3\u2010IFN) and are believed to be necessary to maintain the psoriatic phenotype. In normal KC, \u03b3\u2010IFN is a potent inhibitor of proliferation, but proliferation of KC persists in psoriatic plaques despite the presence of \u03b3\u2010IFN. Immunostaining of interferon regulatory factor\u20101 (IRF\u20101) revealed that IRF\u20101 was localized to the basal cells of the epidermis in normal and in nonlesional psoriatic skin, but was suprabasal or completely absent in lesional psoriatic skin. This finding led to the hypothesis that abnormal signaling in the \u03b3\u2010IFN pathway may occur in psoriatic KC. To test this hypothesis, we measured activation of IRF\u20101 and signal transducer and activator of transcription (STAT)\u20101\u03b1 transcription factors in KC after stimulation with \u03b3\u2010IFN. Primary cultures of KC from normal and nonlesional psoriatic skin were stimulated with \u03b3\u2010IFN and subsequent transcription factor activation was measured by electrophoretic mobility shift assay. Psoriatic KC showed a reduced induction of IRF\u20101 and STAT\u20101\u03b1 activation after stimulation with \u03b3\u2010IFN, compared with normal KC. Reduced activation of IRF\u20101 and STAT\u20101o in response to \u03b3\u2010IFN indicates a fundamental defect in the growth and differentiation control of psoriatic KC in the absence of the influence of other cell types.\u2014Jackson, M., Howie, S. E. M., Weller, R., Sabin, E., Hunter, J. A. A., McKenzie, R. C. Psoriatic keratinocytes show reduced IRF\u20101 and STAT 1\u2010o activation in response to \u03b3\u2010IFN.\n                    <jats:italic>FASEB J.<\/jats:italic>\n                    13, 495\u2013502 (1999)\n                  <\/jats:p>","DOI":"10.1096\/fasebj.13.3.495","type":"journal-article","created":{"date-parts":[[2018,1,18]],"date-time":"2018-01-18T07:34:17Z","timestamp":1516260857000},"page":"495-502","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Psoriatic keratinocytes show reduced IRF\u20101 and STAT\u20101\u03b1 activation in response to \u03b3\u2010IFN"],"prefix":"10.1096","volume":"13","author":[{"given":"Melany","family":"Jackson","sequence":"first","affiliation":[{"name":"Department of Dermatology University of Edinburgh  Edinburgh EH3 9YW Scotland U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah E. 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