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The variation in genetic risk association is likely linked to different HLA class II loci susceptibility, but association studies of HLA class I alleles are scarce. The aim was to investigate HLA class I <jats:italic>A<\/jats:italic>, <jats:italic>B<\/jats:italic>, and <jats:italic>C<\/jats:italic> alleles polymorphisms in children with only T1D, CD, and a subgroup with both T1D and CD (T1D w\/CD).<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and methods<\/jats:title><jats:p>HLA class I <jats:italic>A<\/jats:italic>, <jats:italic>B<\/jats:italic>, and <jats:italic>C<\/jats:italic> genes were genotyped using next\u2010generation targeted sequencing. A conditional analysis was performed on 68 children with T1D, 219 children with CD and seven children with T1D w\/CD enrolled from a birth cohort study at high genetic risk children from the South of Sweden.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Among 1764 HLA class I allele variants, <jats:italic>A*29<\/jats:italic>:<jats:italic>02<\/jats:italic>:<jats:italic>01<\/jats:italic> in T1D w\/CD was associated with both T1D (OR\u00a0=\u00a021.42 [1.05, 1322.4], <jats:italic>p<\/jats:italic>\u00a0=\u20090.0231) and CD (OR\u00a0=\u00a035 [2.36, 529.12], <jats:italic>p<\/jats:italic>\u00a0=\u20090.0051) along with <jats:italic>C*05<\/jats:italic>:<jats:italic>01<\/jats:italic>:<jats:italic>01<\/jats:italic> with both T1D (OR\u00a0=\u00a05.54 [1.06, 24.8], <jats:italic>p<\/jats:italic>\u00a0=\u20090.02) and CD (OR\u00a0=\u00a06.84 [1.46, 26.01], <jats:italic>p<\/jats:italic>\u00a0=\u20090.0077). No independent effects of HLA\u2010B allele associations were observed in T1D w\/CD.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Although the distribution of HLA class I alleles differs between children with T1D and CD, the <jats:italic>A*29<\/jats:italic>:<jats:italic>02<\/jats:italic>:<jats:italic>01<\/jats:italic> and <jats:italic>C*05<\/jats:italic>:<jats:italic>01<\/jats:italic>:<jats:italic>01<\/jats:italic> alleles showed shared risk association of both diseases.<\/jats:p><\/jats:sec>","DOI":"10.1111\/tan.14280","type":"journal-article","created":{"date-parts":[[2021,4,22]],"date-time":"2021-04-22T15:51:30Z","timestamp":1619106690000},"page":"505-511","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["High\u2010resolution genotyping of <scp>HLA<\/scp> class I loci in children with type 1 diabetes and celiac disease"],"prefix":"10.1111","volume":"97","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0536-3535","authenticated-orcid":false,"given":"Shehab","family":"Alshiekh","sequence":"first","affiliation":[{"name":"Department of Clinical Sciences Lund University  Malm\u00f6 Sweden"},{"name":"Department of Medicine King Abdulaziz University  Jeddah Saudi Arabia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniel E.","family":"Geraghty","sequence":"additional","affiliation":[{"name":"Clinical Research Division Fred Hutchinson Cancer Research Center  Seattle Washington USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1435-1234","authenticated-orcid":false,"given":"Daniel","family":"Agardh","sequence":"additional","affiliation":[{"name":"Department of Clinical Sciences Lund University  Malm\u00f6 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