{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,13]],"date-time":"2025-10-13T09:05:00Z","timestamp":1760346300913},"reference-count":51,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2013,1,31]],"date-time":"2013-01-31T00:00:00Z","timestamp":1359590400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2013,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Non\u2010classical human leucocyte antigen\u2010<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>) mediates natural killer and <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8+ <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell activity, suggesting a role in the regulation of autoimmunity.\u00a0<jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>*0103<jats:styled-content style=\"fixed-case\">X<\/jats:styled-content>\/*0103<jats:styled-content style=\"fixed-case\">X<\/jats:styled-content> has been associated with <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>ehcet's disease and <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content> *0101\/*0103<jats:styled-content style=\"fixed-case\">X<\/jats:styled-content> with childhood onset diabetes. We investigated <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content> allele status in 52 <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>aucasian and <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>shkenazi Jewish <jats:styled-content style=\"fixed-case\">P<\/jats:styled-content>emphigus vulgaris (<jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>) patients and 51 healthy controls by restriction fragment length polymorphism\u2013polymerase chain reaction and amplification refractory mutation system. Associations were determined via chi\u2010square test, Fisher's exact test and logistical regression analysis. <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content> outcomes included presumed homozygous *0101\/*0101 or *0103<jats:styled-content style=\"fixed-case\">X<\/jats:styled-content>\/*0103<jats:styled-content style=\"fixed-case\">X<\/jats:styled-content> genotype status or *0101\/*0103<jats:styled-content style=\"fixed-case\">X<\/jats:styled-content> heterozygous status. <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content> did not significantly associate with either *0101\/*0101 or *0101\/*0103<jats:styled-content style=\"fixed-case\">X<\/jats:styled-content> genotypes. <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>*0103<jats:styled-content style=\"fixed-case\">X<\/jats:styled-content>\/*0103<jats:styled-content style=\"fixed-case\">X<\/jats:styled-content> (presumed homozygote) is significantly increased in patients with <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content> versus controls (<jats:italic>P<\/jats:italic>\u00a0=\u00a00.0146, <jats:styled-content style=\"fixed-case\">OR<\/jats:styled-content>\u00a0=\u00a03.730, 95%<jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\u00a0=\u00a01.241\u201311.213). Our data provide the first evidence that <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">E<\/jats:styled-content>*0103<jats:styled-content style=\"fixed-case\">X<\/jats:styled-content> is a marker for genetic risk in <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/exd.12077","type":"journal-article","created":{"date-parts":[[2012,12,21]],"date-time":"2012-12-21T19:15:45Z","timestamp":1356117345000},"page":"108-112","source":"Crossref","is-referenced-by-count":21,"title":["<scp>HLA<\/scp>\u2010<scp>E<\/scp>*0103<scp>X<\/scp> is associated with susceptibility to <scp>P<\/scp>emphigus vulgaris"],"prefix":"10.1111","volume":"22","author":[{"given":"Dhaval G.","family":"Bhanusali","sequence":"first","affiliation":[{"name":"Department of Dermatology University at Buffalo and Roswell Park Cancer Institute State University of New York at Buffalo Buffalo NY 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Chaun","family":"Tong","sequence":"additional","affiliation":[{"name":"Institute for High Performance Computing Connexis Singapore"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kristina","family":"Seiffert\u2010Sinha","sequence":"additional","affiliation":[{"name":"Department of Dermatology University at Buffalo and Roswell Park Cancer Institute State University of New York at Buffalo Buffalo NY USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Animesh A.","family":"Sinha","sequence":"additional","affiliation":[{"name":"Department of Dermatology University at Buffalo and Roswell Park Cancer Institute State University of New York at Buffalo Buffalo NY 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