{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T00:04:55Z","timestamp":1761609895262},"reference-count":52,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2012,7,10]],"date-time":"2012-07-10T00:00:00Z","timestamp":1341878400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2012,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Collagen <jats:styled-content style=\"fixed-case\">XVII<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>17), a transmembrane protein expressed in epidermal keratinocytes (<jats:styled-content style=\"fixed-case\">EK<\/jats:styled-content>), is targeted by pathogenic autoantibodies in bullous pemphigoid. Treatment of <jats:styled-content style=\"fixed-case\">EK<\/jats:styled-content> with anti\u2010<jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>17 autoantibodies triggers the production of proinflammatory cytokines. In this study, we test the hypothesis that <jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>17 is involved in the regulation of the <jats:styled-content style=\"fixed-case\">EK<\/jats:styled-content> proinflammatory response, using <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108 expression as the primary readout. The absence of <jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>17 in <jats:styled-content style=\"fixed-case\">EK<\/jats:styled-content> derived from a junctional epidermolysis bullosa patient or sh<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010mediated knockdown of <jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>17 in normal <jats:styled-content style=\"fixed-case\">EK<\/jats:styled-content> resulted in a dysregulation of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108 responses under various conditions. The <jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>17\u2010deficient cells showed an abnormally high <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108 response after treatment with lipopolysaccharide (<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>), ultraviolet\u2010B radiation or tumor necrosis factor, but exhibited a blunted <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108 response to phorbol 12\u2010myristate 13\u2010acetate exposure. Induction of <jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>17 expression in <jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>17\u2010negative <jats:styled-content style=\"fixed-case\">EK<\/jats:styled-content> led to a normalization of the <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010induced proinflammatory response. Although \u03b16\u03b24 integrin was found to be up\u2010regulated in <jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>17\u2010deficient <jats:styled-content style=\"fixed-case\">EK<\/jats:styled-content>, si<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010mediated knockdown of the \u03b16 and \u03b24 subunits revealed that <jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>17's effects on the <jats:styled-content style=\"fixed-case\">LPS IL<\/jats:styled-content>\u20108 response are not dependent on this integrin. In <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010treated cells, inhibition of <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010kappa B activity in <jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>17\u2010negative <jats:styled-content style=\"fixed-case\">EK<\/jats:styled-content> resulted in a normalization of their <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108 response, and expression of an <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010kappa B\u2010driven reporter was shown to be higher in <jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>17\u2010deficient, compared with normal <jats:styled-content style=\"fixed-case\">EK<\/jats:styled-content>. These findings support the hypothesis that <jats:styled-content style=\"fixed-case\">COL<\/jats:styled-content>17 plays an important regulatory role in the <jats:styled-content style=\"fixed-case\">EK<\/jats:styled-content> proinflammatory response, acting largely via <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010kappa B. Future investigations will focus on further defining the molecular basis of this novel control network.<\/jats:p>","DOI":"10.1111\/j.1600-0625.2012.01529.x","type":"journal-article","created":{"date-parts":[[2012,5,10]],"date-time":"2012-05-10T14:23:24Z","timestamp":1336659804000},"page":"605-611","source":"Crossref","is-referenced-by-count":28,"title":["Collagen <scp>XVII<\/scp> (<scp>BP<\/scp>180) modulates keratinocyte expression of the proinflammatory chemokine, <scp>IL<\/scp>\u20108"],"prefix":"10.1111","volume":"21","author":[{"given":"Fran\u00e7oise","family":"Van den Bergh","sequence":"first","affiliation":[{"name":"Division of Rheumatology Medical College of Wisconsin Milwaukee WI USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steven L.","family":"Eliason","sequence":"additional","affiliation":[{"name":"Department of Dermatology University of Iowa Carver College of Medicine Iowa City IA 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