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Different cytokines have been implicated in the disease profile, but their pathogenic role is not yet fully determined. We studied biopsies of pretreatment lesional and non\u2010lesional (<jats:styled-content style=\"fixed-case\">NL<\/jats:styled-content>) scalp and post\u2010treatment (intra\u2010lesional steroid injection) lesional scalp of 6 patchy patients with <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> using immunohistochemistry and gene expression analysis. Immunohistochemistry showed increases in <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>3<jats:sup>+<\/jats:sup>, <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8<jats:sup>+<\/jats:sup> T cells, <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>11c<jats:sup>+<\/jats:sup> dendritic cells and <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>1a<jats:sup>+<\/jats:sup> Langerhans cells within and around hair follicles of pretreatment lesional scalp, which decreased upon treatment. <jats:styled-content style=\"fixed-case\">qRT<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content> showed in pretreatment lesional scalp (compared to <jats:styled-content style=\"fixed-case\">NL<\/jats:styled-content>) significant increases (<jats:italic>P<\/jats:italic> &lt; 0.05) in expression of inflammatory markers (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20102, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20102<jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> JAK<\/jats:styled-content>3, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201015), Th1 (<jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>10 and <jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>9), Th2 (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201013, <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>17 and <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>18), <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201012\/<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201023p40 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201032. Among these, we observed significant downregulation with treatment in <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201012\/<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201023p40, <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>18 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201032. We also observed significant downregulation of several hair keratins in lesional scalp, with significant upregulation of <jats:styled-content style=\"fixed-case\">KRT<\/jats:styled-content>35, <jats:styled-content style=\"fixed-case\">KRT<\/jats:styled-content>75 and <jats:styled-content style=\"fixed-case\">KRT<\/jats:styled-content>86 in post\u2010treatment lesional scalp. This study shows concurrent activation of Th1 and Th2 immune axes as well as <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201023 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201032 cytokine pathways in lesional <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> scalp and defined a series of response biomarkers to corticosteroid injection. Clinical trials with selective antagonists coupled with cytokine\u2010pathway biomarkers will be necessary to further dissect pathogenic immunity.<\/jats:p>","DOI":"10.1111\/exd.12918","type":"journal-article","created":{"date-parts":[[2015,12,14]],"date-time":"2015-12-14T13:18:16Z","timestamp":1450099096000},"page":"282-286","source":"Crossref","is-referenced-by-count":84,"title":["Biomarkers of alopecia areata disease activity and response to corticosteroid treatment"],"prefix":"10.1111","volume":"25","author":[{"given":"Judilyn","family":"Fuentes\u2010Duculan","sequence":"first","affiliation":[{"name":"Laboratory for Investigative Dermatology The Rockefeller University New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas","family":"Gulati","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology The Rockefeller University New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathleen M.","family":"Bonifacio","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology The Rockefeller University New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Norma","family":"Kunjravia","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology The Rockefeller University New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiuzhong","family":"Zheng","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology The Rockefeller University New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mayte","family":"Su\u00e1rez\u2010Fari\u00f1as","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology The Rockefeller University New York NY USA"},{"name":"Dermatology Department Icahn School of Medicine at Mount Sinai New York NY USA"},{"name":"Department of Population Health Science and 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