{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,13]],"date-time":"2025-10-13T09:06:01Z","timestamp":1760346361138},"reference-count":46,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2014,2,11]],"date-time":"2014-02-11T00:00:00Z","timestamp":1392076800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Alcoholism Clin &amp;amp; Exp Res"],"published-print":{"date-parts":[[2014,5]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Chronic alcoholism is associated with increased incidence and severity of cutaneous infection. Skin\u2010resident T cells orchestrate numerous immunological functions that are critically involved in both tissue homeostasis and cutaneous immunity. The impact of chronic ethanol (Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content>) exposure on skin T cells has not previously been examined; given their important role in maintaining the immune barrier function of the skin further study is warranted.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Mice were administered Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> in the drinking water for 12 to 16\u00a0weeks. Flow cytometry was used to evaluate impact of Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> feeding on skin T cell numbers, rates of proliferation, and apoptosis as well as activation marker expression and cytokine production after ex vivo stimulation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Chronic Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> feeding caused a baseline reduction in dendritic epidermal T cell (<jats:styled-content style=\"fixed-case\">DETC<\/jats:styled-content>) numbers that corresponded with reduced expression of the activation marker <jats:styled-content style=\"fixed-case\">JAML<\/jats:styled-content> following phorbol 12\u2010myristate 13\u2010acetate (<jats:styled-content style=\"fixed-case\">PMA<\/jats:styled-content>)\/ionomycin stimulation. Chronic Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> feeding did not alter total numbers of dermal T cells, but specific subset loss was observed in Foxp3<jats:sup>+<\/jats:sup> regulatory T cells (Tregs) as well as <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>3hi, V\u03b33<jats:sup>+<\/jats:sup> and <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>3int, V\u03b33<jats:sup>\u2212<\/jats:sup> dermal \u03b3\u03b4 T cells. Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content>\u2010induced dysfunction in the latter population, which represents prototypical interleukin\u201017 (IL\u201017)\u2010producing dermal \u03b3\u03b4T17s, was made evident by diminished <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 production following anti\u2010<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>3 stimulation. Additionally, the capacity of lymph node \u03b3\u03b4 T cells to produce <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 following anti\u2010<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>3 and <jats:styled-content style=\"fixed-case\">PMA<\/jats:styled-content>\/ionomycin stimulation was impaired by chronic Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> feeding.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Chronic Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> feeding induced defects in both numbers and function of multiple skin T cell subsets. The decreased density and poor responsiveness of <jats:styled-content style=\"fixed-case\">DETC<\/jats:styled-content>s and \u03b3\u03b4T17 cells in particular would be expected to compromise immune effector mechanisms necessary to maintain a protective barrier and restrict pathogen invasion. These findings demonstrate the sensitivity of skin T cells to Et<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content> and provide new mechanisms to help explain the propensity of alcoholics to suffer skin infection.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.12358","type":"journal-article","created":{"date-parts":[[2014,2,12]],"date-time":"2014-02-12T10:35:03Z","timestamp":1392201303000},"page":"1356-1364","source":"Crossref","is-referenced-by-count":18,"title":["Chronic Ethanol Feeding Induces Subset Loss and Hyporesponsiveness in Skin T Cells"],"prefix":"10.1111","volume":"38","author":[{"given":"Corey P.","family":"Parlet","sequence":"first","affiliation":[{"name":"Department of Pathology and Interdisciplinary Graduate Program in Immunology University of Iowa Carver College of Medicine Iowa City Iowa"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas J.","family":"Waldschmidt","sequence":"additional","affiliation":[{"name":"Department of Pathology and Interdisciplinary Graduate Program in Immunology University of Iowa Carver College of Medicine Iowa City Iowa"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Annette J.","family":"Schlueter","sequence":"additional","affiliation":[{"name":"Department of Pathology and Interdisciplinary Graduate Program in Immunology University of Iowa Carver College of Medicine Iowa City 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