{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,6,25]],"date-time":"2024-06-25T15:18:18Z","timestamp":1719328698448},"reference-count":29,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2016,2,10]],"date-time":"2016-02-10T00:00:00Z","timestamp":1455062400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000871","name":"Mayo Clinic","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000871","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01GM103841","R01AR056635"],"award-info":[{"award-number":["R01GM103841","R01AR056635"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2016,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Aiming to decipher immunological mechanisms of the autoimmune disorder alopecia areata (<jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>), we hypothesized that interleukin\u20106 (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106) might be associated with juvenile\u2010onset <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>, for which there is currently no experimental model. Upon intramuscular transgenesis to overexpress <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 in pregnant female C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6 (B6) mice, we found that the offspring displayed an initial normal and complete juvenile hair growth cycle, but developed alopecia around postnatal day 18. This alopecia was patchy and reversible (non\u2010scarring) and was associated with upregulation of <jats:italic>Ulbp1<\/jats:italic> expression, the only mouse homolog of the human <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>\u2010associated <jats:styled-content style=\"fixed-case\">ULBP<\/jats:styled-content>3 gene. Alopecia was also associated with inflammatory infiltration of hair follicles by lymphocytes, including alpha\u2010beta T cells, which contributed to surface hair loss. Despite these apparently shared traits with <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>, lesions were dominated by follicular dystrophy that was atypical of human <jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content> disease, sharing some traits consistent with B6 alopecia and dermatitis. Additionally, juvenile\u2010onset alopecia was followed by complete, spontaneous recovery of surface hair, without recurrence of hair loss. Prolonging exposure to <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 prolonged the time to recovery, but once recovered, repeating high\u2010dose <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 exposure <jats:italic>de novo<\/jats:italic> did not re\u2010induce alopecia. These data suggest that although substantial molecular and cellular pathways may be shared, functionally similar alopecia disorders can occur via distinct pathological mechanisms.<\/jats:p>","DOI":"10.1111\/exd.12914","type":"journal-article","created":{"date-parts":[[2015,12,14]],"date-time":"2015-12-14T11:27:11Z","timestamp":1450092431000},"page":"223-228","source":"Crossref","is-referenced-by-count":3,"title":["Maternal <scp>IL<\/scp>\u20106 can cause T\u2010cell\u2010mediated juvenile alopecia by non\u2010scarring follicular dystrophy in mice"],"prefix":"10.1111","volume":"25","author":[{"given":"Stephen E. P.","family":"Smith","sequence":"first","affiliation":[{"name":"Department of Immunology Mayo Clinic College of Medicine Rochester MN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rachel L. 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