{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:09:13Z","timestamp":1787015353820,"version":"build-2736575974"},"reference-count":19,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2018,11,28]],"date-time":"2018-11-28T00:00:00Z","timestamp":1543363200000},"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":["Acad Dermatol Venereol"],"published-print":{"date-parts":[[2019,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Bullous pemphigoid (\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      ) is the most common autoimmune blistering disease.\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      180 is the primary autoantigen of\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      , and in a portion of\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      cases,\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230 is the only target of autoantibodies. Such\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      is called\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      .\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      tends to show milder clinical phenotypes than conventional\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      , but the reason is unclear. The pathogenic roles of autoantibodies and complement activation have been shown in conventional\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      , but the distribution of IgG subclasses and the degree of complement deposition in\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      remain unclear.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      To compare the distribution of IgG subclasses and the degree of complement deposition in\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      with those in conventional\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      with autoantibodies to\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      180 and\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230 (\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      180\u2010\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      ).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The diagnosis of\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      was confirmed by the histopathology of the lesions, the deposition of IgG and complement in the perilesional skin and the presence of circulating autoantibodies to\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      180 and\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230. The disease severity was determined by bullous pemphigoid disease area index. The deposition of IgG subclasses and complement deposition were examined by direct immunofluorescence of the perilesional skin in 6\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      cases and 11\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      180\u2010\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      cases.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Sixty seven percent of\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      cases show a mild clinical phenotype. All\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      cases and 82% of\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      180\u2010\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      cases were found to demonstrate the clear deposition of IgG4 at the basement membrane zone of skin specimens. Notably, the deposition of IgG1 and IgG3 was faint or negative in all of the\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      cases, whereas they were clearly detected in 91% and 64% of the\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      180\u2010\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      cases, respectively. The deposition of complement C3 tended to be weaker in\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      than in\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      180\u2010\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      The mild clinical phenotype of\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      230\u2010type\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      may correlate with the weaker deposition of IgG1, IgG3 and complement in the skin lesions.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jdv.15325","type":"journal-article","created":{"date-parts":[[2018,11,5]],"date-time":"2018-11-05T06:42:59Z","timestamp":1541400179000},"page":"595-600","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Characteristics of IgG subclasses and complement deposition in\n                    <scp>BP<\/scp>\n                    230\u2010type bullous pemphigoid"],"prefix":"10.1111","volume":"33","author":[{"given":"M.","family":"Zheng","sequence":"first","affiliation":[{"name":"Department of Dermatology Hokkaido University Graduate School of Medicine Sapporo 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