{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T20:13:48Z","timestamp":1773864828789,"version":"3.50.1"},"reference-count":50,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2018,7,6]],"date-time":"2018-07-06T00:00:00Z","timestamp":1530835200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004332","name":"Seoul National University Hospital","doi-asserted-by":"publisher","award":["04\u20102008\u20100730"],"award-info":[{"award-number":["04\u20102008\u20100730"]}],"id":[{"id":"10.13039\/501100004332","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acad Dermatol Venereol"],"published-print":{"date-parts":[[2018,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Fibrosis is thought to be the main pathophysiology of scleroderma, and myofibroblasts play the main role in abnormal fibrotic pathologies. Altered distribution of dermal dendritic cells (<jats:styled-content style=\"fixed-case\">DDC<\/jats:styled-content>s) and vascular abnormalities has been reported to relate to the pathogenesis of scleroderma.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objective<\/jats:title><jats:p>To investigate fibrotic pathogenesis of morphea (localized scleroderma) by demonstrating the relative expression and distribution of <jats:styled-content style=\"fixed-case\">DDC<\/jats:styled-content>s and myofibroblasts, we performed immunohistochemical stains using several relevant antibodies.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Skin lesions of 50 patients with morphea and age\u2010, sex\u2010 and site\u2010matched normal skin of 50 subjects were evaluated for the following antibodies: <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>34, factor <jats:styled-content style=\"fixed-case\">XIII<\/jats:styled-content>a (<jats:styled-content style=\"fixed-case\">FXIII<\/jats:styled-content>a), smooth muscle actin (<jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content>), <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>31 and vascular cell adhesion molecule\u20101 (<jats:styled-content style=\"fixed-case\">VCAM<\/jats:styled-content>\u20101).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>34 stromal stain was significantly lower in patients than controls (<jats:italic>P<\/jats:italic> = 0.000), while <jats:styled-content style=\"fixed-case\">FXIII<\/jats:styled-content>a, <jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">VCAM<\/jats:styled-content>\u20101 stains were significantly higher in patients than controls (<jats:italic>P<\/jats:italic> = 0.043, <jats:italic>P<\/jats:italic> = 0.000 and <jats:italic>P<\/jats:italic> = 0.027, respectively). In subtype analysis within patients, <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>34 stromal stain showed decreasing trends with increasing disease extent and increasing fibrosis, respectively. <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>34 stromal stain showed an inverse correlation and mutually exclusive spatial expression pattern with <jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content> stain (<jats:italic>r<\/jats:italic> = \u22120.286, <jats:italic>P<\/jats:italic> = 0.044). The inverse relationship was maintained in each dermal layer analysis, upper and lower dermis (<jats:italic>r<\/jats:italic> = \u22120.397, <jats:italic>P<\/jats:italic> = 0.004 and <jats:italic>r<\/jats:italic> = \u22120.281, <jats:italic>P<\/jats:italic> = 0.048, respectively).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Mutually exclusive staining patterns of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>34 stromal and <jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content> stains suggest a phenotypic change of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>34+ <jats:styled-content style=\"fixed-case\">DDC<\/jats:styled-content>s into <jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content>+ myofibroblasts with increasing disease extent and fibrosis in morphea. Degree of loss of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>34+ <jats:styled-content style=\"fixed-case\">DDC<\/jats:styled-content>s can be a useful marker in predicting the extent and severity of morphea.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jdv.15120","type":"journal-article","created":{"date-parts":[[2018,6,11]],"date-time":"2018-06-11T03:54:45Z","timestamp":1528689285000},"page":"2208-2216","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["<scp>CD<\/scp>34 stromal expression is inversely proportional to smooth muscle actin expression and extent of morphea"],"prefix":"10.1111","volume":"32","author":[{"given":"J.S.","family":"Lee","sequence":"first","affiliation":[{"name":"Department of Dermatology Seoul Metropolitan Government \u2010 Seoul National University Boramae Medical Center Seoul Korea"},{"name":"Institute of Human\u2010Environmental Interface Biology Medical Research Center 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