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It includes various agonists and two antagonists, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>a and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>a. Our aim was to investigate whether the <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 family is involved in allergic contact dermatitis (<jats:styled-content style=\"fixed-case\">ACD<\/jats:styled-content>). The expression of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 family members was evaluated by <jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content> and immunohistochemistry in the positive patch test reaction site (involved skin) and in the uninvolved skin of <jats:styled-content style=\"fixed-case\">ACD<\/jats:styled-content> patients. We also examined these cytokines in an <jats:italic>ex vivo<\/jats:italic> model of <jats:styled-content style=\"fixed-case\">ACD<\/jats:styled-content>. The antagonistic activity of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>a was evaluated by injecting recombinant <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>a in uninvolved skin biopsies of <jats:styled-content style=\"fixed-case\">ACD<\/jats:styled-content> patients. <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>a and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>a expression was quantified in mononuclear cells of nickel\u2010sensitized patients challenged <jats:italic>in vitro<\/jats:italic> with nickel. <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033 involvement in <jats:styled-content style=\"fixed-case\">ACD<\/jats:styled-content> was investigated by intra\u2010dermal injection of anti\u2010<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033 in the uninvolved skin of patients <jats:italic>ex vivo<\/jats:italic>. Results showed that <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>a, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036\u03b1, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036\u03b2, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036\u03b3 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033 expression, but not <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>a expression, was enhanced in <jats:styled-content style=\"fixed-case\">ACD<\/jats:styled-content>\u2010involved skin. Immunohistochemical analysis and <jats:italic>ex vivo<\/jats:italic> skin cultures confirmed these results. Injection of anti\u2010<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033 in <jats:styled-content style=\"fixed-case\">ACD<\/jats:styled-content>\u2010uninvolved skin inhibited <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108 expression, whereas <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>a inhibited <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036\u03b1, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036\u03b2, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201036\u03b3 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108 expression. Nickel induced <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>a expression in lymphocytes of nickel\u2010sensitized patients. Hence, various <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 agonists and antagonists may be involved in <jats:styled-content style=\"fixed-case\">ACD<\/jats:styled-content> pathogenesis.<\/jats:p>","DOI":"10.1111\/exd.12272","type":"journal-article","created":{"date-parts":[[2013,10,24]],"date-time":"2013-10-24T14:03:58Z","timestamp":1382623438000},"page":"813-819","source":"Crossref","is-referenced-by-count":69,"title":["The balance between pro\u2010 and anti\u2010inflammatory cytokines is crucial in human allergic contact dermatitis pathogenesis: the role of IL\u20101 family members"],"prefix":"10.1111","volume":"22","author":[{"given":"Martina","family":"Mattii","sequence":"first","affiliation":[{"name":"Department of Dermatology University of Naples Federico II School of Medicine Naples Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabio","family":"Ayala","sequence":"additional","affiliation":[{"name":"Department of Dermatology 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