{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:43:28Z","timestamp":1787013808067,"version":"build-2736575974"},"reference-count":25,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2017,2,17]],"date-time":"2017-02-17T00:00:00Z","timestamp":1487289600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Aust J Dermatology"],"published-print":{"date-parts":[[2017,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Autoantibodies to the desmosomal proteins desmoglein 1 and 3 cause pemphigus foliaceus and pemphigus vulgaris, which are characterised by keratinocyte dissociation (acantholysis) and intraepidermal blister formation. The passive transfer of pathogenic anti\u2010desmoglein antibodies induces blisters in mice\n                    <jats:italic>in vivo<\/jats:italic>\n                    and the loss of keratinocyte adhesion\n                    <jats:italic>in vitro<\/jats:italic>\n                    . The pathogenetic mechanisms of acantholysis due to anti\u2010desmoglein autoantibodies are not fully understood. However, recent studies have revealed that signalling\u2010dependent and signalling\u2010independent pathways are operative in the loss of cell adhesion. In this review, we focus on the pathomechanism of acantholysis due to autoantibodies to desmogleins and recent therapeutic approaches.\n                  <\/jats:p>","DOI":"10.1111\/ajd.12562","type":"journal-article","created":{"date-parts":[[2017,2,17]],"date-time":"2017-02-17T02:22:44Z","timestamp":1487298164000},"page":"171-173","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Pemphigus, a pathomechanism of acantholysis"],"prefix":"10.1111","volume":"58","author":[{"given":"Masutaka","family":"Furue","sequence":"first","affiliation":[{"name":"Department of Dermatology Kyushu University Fukuoka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takafumi","family":"Kadono","sequence":"additional","affiliation":[{"name":"Department of Dermatology St Marianna University School of Medicine Kawasaki Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,2,17]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a002543"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20100567"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00441-015-2136-5"},{"key":"e_1_2_5_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceb.2014.10.004"},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra061111"},{"key":"e_1_2_5_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceb.2004.07.006"},{"key":"e_1_2_5_8_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2133.2012.10827.x"},{"key":"e_1_2_5_9_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-0960.2012.00921.x"},{"key":"e_1_2_5_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.clindermatol.2011.01.014"},{"key":"e_1_2_5_11_1","doi-asserted-by":"publisher","DOI":"10.1111\/1346-8138.13041"},{"key":"e_1_2_5_12_1","doi-asserted-by":"publisher","DOI":"10.1111\/1346-8138.13230"},{"key":"e_1_2_5_13_1","doi-asserted-by":"publisher","DOI":"10.1038\/cddis.2016.147"},{"key":"e_1_2_5_14_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.181.3.1825"},{"key":"e_1_2_5_15_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0050696"},{"key":"e_1_2_5_16_1","first-page":"800","article-title":"Peptide\u2010mediated desmoglein 3 crosslinking prevents pemphigus vulgaris autoantibody\u2010induced skin blistering","volume":"123","author":"Spindler V","year":"2013","journal-title":"J. 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