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Low\u2010resolution <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010A, \u2010Cw and \u2010<jats:styled-content style=\"fixed-case\">DRB<\/jats:styled-content>1 allele typing was carried out in 86 families comprising 339 individuals (86 Ro\/<jats:styled-content style=\"fixed-case\">SSA<\/jats:styled-content> autoantibody\u2010positive mothers, 71 fathers, 87 <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> index cases and 95 unaffected siblings).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>A case\u2013control comparison between index cases and population\u2010based out\u2010of\u2010study controls (<jats:italic>n<\/jats:italic>\u00a0=\u00a01710) revealed association of <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> with 15 <jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s in the 6p21.3 <jats:styled-content style=\"fixed-case\">MHC<\/jats:styled-content> locus at a chromosome\u2010wide significance of <jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>2.59\u00a0\u00d7\u00a010<jats:sup>\u22126<\/jats:sup> (<jats:styled-content style=\"fixed-case\">OR<\/jats:styled-content> 2.21\u20133.12). In a family\u2010based analysis of association of <jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content> markers as well as distinct <jats:styled-content style=\"fixed-case\">MHC<\/jats:styled-content> class I and <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> alleles with <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">DRB<\/jats:styled-content>1*04 and <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010Cw*05 variants were significantly more frequently transmitted to affected individuals (<jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.03 and <jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.05, respectively), whilst <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">DRB<\/jats:styled-content>1*13 and <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010Cw*06 variants were significantly less often transmitted to affected children (<jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.04 and <jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.03). We further observed marked association of increased paternal (but not maternal) <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">DRB<\/jats:styled-content>1*04 transmission to affected offspring (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.02).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">DRB<\/jats:styled-content>1*04 and <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010Cw*05 were identified as novel foetal <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> allele variants that confer susceptibility to <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> in response to Ro\/<jats:styled-content style=\"fixed-case\">SSA<\/jats:styled-content> autoantibody exposure, whilst <jats:styled-content style=\"fixed-case\">DRB<\/jats:styled-content>1*13 and Cw*06 emerged as protective alleles. Additionally, we demonstrated a paternal contribution to foetal susceptibility to <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> for the first time.<\/jats:p><\/jats:sec>","DOI":"10.1111\/joim.12179","type":"journal-article","created":{"date-parts":[[2013,12,20]],"date-time":"2013-12-20T07:17:25Z","timestamp":1387523845000},"page":"640-651","source":"Crossref","is-referenced-by-count":30,"title":["The <scp>HLA<\/scp> locus contains novel foetal susceptibility alleles for congenital heart block with significant paternal influence"],"prefix":"10.1111","volume":"275","author":[{"given":"S.","family":"Meisgen","sequence":"first","affiliation":[{"name":"Department of Medicine Karolinska Institutet Uppsala University Uppsala Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"\u00d6stberg","sequence":"additional","affiliation":[{"name":"Department of Medicine Karolinska Institutet Uppsala University Uppsala 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