{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T05:47:18Z","timestamp":1768283238467,"version":"3.49.0"},"reference-count":33,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2015,9,28]],"date-time":"2015-09-28T00:00:00Z","timestamp":1443398400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Acad Dermatol Venereol"],"published-print":{"date-parts":[[2015,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Alopecia areata (<jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>) is a T\u2010cell\u2010driven autoimmune disease of the hair follicle and frequently reported to be associated with inflammatory skin diseases (<jats:styled-content style=\"fixed-case\">ISD<\/jats:styled-content>) such as atopic eczema (<jats:styled-content style=\"fixed-case\">AE<\/jats:styled-content>) or psoriasis. Interestingly, <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> on the one hand and both <jats:styled-content style=\"fixed-case\">AE<\/jats:styled-content> and psoriasis on the other hand are believed to be driven by mutually antagonistic T\u2010cell subsets.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objective<\/jats:title><jats:p>To characterize <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>\u2010specific T\u2010cell profiles and inflammatory pattern by intra\u2010individual comparison of <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> and coexistent <jats:styled-content style=\"fixed-case\">ISD<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>112 patients with <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> were recruited and investigated for coexisting <jats:styled-content style=\"fixed-case\">ISD<\/jats:styled-content>. In\u2010depth analyses were performed in patients with <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">AE<\/jats:styled-content> (<jats:italic>n<\/jats:italic> = 2), <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> and psoriasis (<jats:italic>n<\/jats:italic> = 1), <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> and psoriasis and <jats:styled-content style=\"fixed-case\">AE<\/jats:styled-content> (<jats:italic>n<\/jats:italic> = 1) and <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> and lichen planus (<jats:italic>n<\/jats:italic> = 1), using histology, immunohistochemistry and cytokine staining of T cells isolated from lesional skin.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Of 112 <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> patients investigated, 23 suffered from an <jats:styled-content style=\"fixed-case\">ISD<\/jats:styled-content>. The prevalence of <jats:styled-content style=\"fixed-case\">AE<\/jats:styled-content>, vitiligo, psoriasis and lichen planus was higher in the investigated <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> cohort than in the normal population. The clinical as well as histological phenotype of <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> the coexistent <jats:styled-content style=\"fixed-case\">ISD<\/jats:styled-content> were unequivocal. In line with this, T\u2010cell infiltrates were found to be disease\u2010characteristics with <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> and lichen planus dominated by <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8+ and <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3+ <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1+ producing T cells while psoriasis lesions in the same patients were dominated by <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017+ and <jats:styled-content style=\"fixed-case\">AE<\/jats:styled-content> by <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20104+ T cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> patients have a higher incidence of various T\u2010cell\u2010driven inflammatory skin diseases than the normal population, a phenomenon which might relate to over\u2010activation of skin\u2010homing T cells and to specific immune triggers as the primary cause of inflammation. More importantly, we showed that by using <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> as a model disease, our approach of intra\u2010individual comparison of distinct inflammatory responses in the same patient is feasible and offers the unique possibility to gain insights into disease pathogenesis independent from genetic susceptibilities.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jdv.13325","type":"journal-article","created":{"date-parts":[[2015,9,29]],"date-time":"2015-09-29T00:56:06Z","timestamp":1443488166000},"page":"2429-2435","source":"Crossref","is-referenced-by-count":19,"title":["Dissecting susceptibility from exogenous triggers: the model of alopecia areata and associated inflammatory skin diseases"],"prefix":"10.1111","volume":"29","author":[{"given":"N.","family":"Garzorz","sequence":"first","affiliation":[{"name":"Department of Dermatology and Allergy Technical University of Munich Munich 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