{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T13:21:24Z","timestamp":1777036884112,"version":"3.51.4"},"reference-count":41,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2014,5,28]],"date-time":"2014-05-28T00:00:00Z","timestamp":1401235200000},"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":[[2014,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Atopic dermatitis is a chronic inflammatory disease characterized by an impaired epidermal barrier function combined with a chronic Th2\u2010type inflammatory response and an intense pruritus. Here, we used an experimental mouse model for Th2\u2010type contact hypersensitivity (<jats:styled-content style=\"fixed-case\">CHS<\/jats:styled-content>) to fluorescein isothiocyanate (<jats:styled-content style=\"fixed-case\">FITC<\/jats:styled-content>) to investigate the potential role of cannabinoid 1 receptors (<jats:styled-content style=\"fixed-case\">CB<\/jats:styled-content>1) in the pathophysiology of mouse atopic\u2010like dermatitis. Mice lacking <jats:styled-content style=\"fixed-case\">CB<\/jats:styled-content>1 receptors globally (Cnr1<jats:sup>\u2212\/\u2212<\/jats:sup>) or specifically in keratinocytes (<jats:styled-content style=\"fixed-case\">KC<\/jats:styled-content>\u2010Cnr1<jats:sup>\u2212\/\u2212<\/jats:sup>) as well as wild\u2010type (<jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>) control mice were sensitized and challenged with <jats:styled-content style=\"fixed-case\">FITC<\/jats:styled-content>. We examined ear swelling responses, transepidermal water loss, Th2\u2010type skin inflammatory responses and serum IgE levels. Both Cnr1<jats:sup>\u2212\/\u2212<\/jats:sup> and <jats:styled-content style=\"fixed-case\">KC<\/jats:styled-content>\u2010Cnr1<jats:sup>\u2212\/\u2212<\/jats:sup> showed enhanced <jats:styled-content style=\"fixed-case\">CHS<\/jats:styled-content> responses to <jats:styled-content style=\"fixed-case\">FITC<\/jats:styled-content> and a delayed epidermal barrier repair when compared with <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice. m<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> levels for <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20104, thymic stromal lymphopoietin (<jats:styled-content style=\"fixed-case\">TSLP<\/jats:styled-content>) and <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>8, as well as eosinophil activity, were significantly increased in inflamed ear tissue of <jats:styled-content style=\"fixed-case\">FITC<\/jats:styled-content>\u2010challenged Cnr1<jats:sup>\u2212\/\u2212<\/jats:sup> and <jats:styled-content style=\"fixed-case\">KC<\/jats:styled-content>\u2010Cnr1<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Importantly, <jats:styled-content style=\"fixed-case\">CB<\/jats:styled-content>1 receptor\u2010deficient keratinocytes secreted increased levels of <jats:styled-content style=\"fixed-case\">TSLP<\/jats:styled-content>, a proinflammatory mediator that drives Th2\u2010type skin inflammation in atopic dermatitis, under basal and Th2\u2010type inflammatory conditions. Taken together, our results demonstrate that <jats:styled-content style=\"fixed-case\">CB<\/jats:styled-content>1 receptors in keratinocytes help to maintain epidermal barrier homoeostasis and attenuate Th2\u2010type allergic inflammatory responses. Based on our work, we propose that enhanced epidermal allergen penetrance cooperates with increased production of <jats:styled-content style=\"fixed-case\">TSLP<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>8 by epidermal keratinocytes for the induction of type 2 <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4+ T helper cells. Our results place keratinocytes at the cross\u2010roads of outside\u2010in and inside\u2010out pathophysiologic mechanisms of atopic dermatitis.<\/jats:p>","DOI":"10.1111\/exd.12414","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T08:30:25Z","timestamp":1398069025000},"page":"401-406","source":"Crossref","is-referenced-by-count":31,"title":["Cannabinoid 1 receptors in keratinocytes attenuate fluorescein isothiocyanate\u2010induced mouse atopic\u2010like dermatitis"],"prefix":"10.1111","volume":"23","author":[{"given":"Evelyn","family":"Gaffal","sequence":"first","affiliation":[{"name":"Department of Dermatology and Allergy Laboratory of Experimental Dermatology University of Bonn Bonn Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nicole","family":"Glodde","sequence":"additional","affiliation":[{"name":"Department of Dermatology and Allergy Laboratory of Experimental Dermatology University of Bonn Bonn Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mira","family":"Jakobs","sequence":"additional","affiliation":[{"name":"Department of Dermatology and Allergy Laboratory of Experimental Dermatology University of Bonn Bonn Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tobias","family":"Bald","sequence":"additional","affiliation":[{"name":"Department of Dermatology and Allergy Laboratory of Experimental Dermatology University of Bonn Bonn Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas","family":"T\u00fcting","sequence":"additional","affiliation":[{"name":"Department of Dermatology and Allergy Laboratory of Experimental Dermatology University of Bonn Bonn 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