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Genetic factors account for approximately 50% of the total risk, with variants in the HLA region contributing to half of this genetic risk. Research has historically focused on populations of European ancestry. We developed HLA-focused type 1 diabetes genetic risk scores (T1D GRS\n                      <jats:sub>HLA<\/jats:sub>\n                      ) using SNPs or HLA alleles from four ancestry groups (admixed African [AFR; T1D GRS\n                      <jats:sub>HLA-AFR<\/jats:sub>\n                      ], admixed American [AMR; T1D GRS\n                      <jats:sub>HLA-AMR<\/jats:sub>\n                      ], European [EUR; T1D GRS\n                      <jats:sub>HLA-EUR<\/jats:sub>\n                      ] and Finnish [FIN; T1D GRS\n                      <jats:sub>HLA-FIN<\/jats:sub>\n                      ]). We also developed an across-ancestry GRS (ALL; T1D GRS\n                      <jats:sub>HLA-ALL<\/jats:sub>\n                      ). We assessed the performance of the GRS in each population to determine the transferability of constructed scores.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      A total of 41,689 samples and 13,695 SNPs in the HLA region were genotyped, with HLA alleles imputed using the HLA-TAPAS multi-ethnic reference panel. Conditionally independent SNPs and HLA alleles associated with type 1 diabetes were identified in each population group to construct T1D GRS\n                      <jats:sub>HLA<\/jats:sub>\n                      models. Generated T1D GRS\n                      <jats:sub>HLA<\/jats:sub>\n                      models were used to predict HLA-focused type 1 diabetes genetic risk across four ancestry groups. The performance of each T1D GRS\n                      <jats:sub>HLA<\/jats:sub>\n                      model was assessed using receiver operating characteristic (ROC) AUCs, and compared statistically.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Each T1D GRS\n                      <jats:sub>HLA<\/jats:sub>\n                      model included a different number of conditionally independent HLA-region SNPs (AFR,\n                      <jats:italic>n<\/jats:italic>\n                      =5; AMR,\n                      <jats:italic>n<\/jats:italic>\n                      =3; EUR,\n                      <jats:italic>n<\/jats:italic>\n                      =38; FIN,\n                      <jats:italic>n<\/jats:italic>\n                      =6; ALL,\n                      <jats:italic>n<\/jats:italic>\n                      =36) and HLA alleles (AFR,\n                      <jats:italic>n<\/jats:italic>\n                      =6; AMR,\n                      <jats:italic>n<\/jats:italic>\n                      =5; EUR,\n                      <jats:italic>n<\/jats:italic>\n                      =40; FIN,\n                      <jats:italic>n<\/jats:italic>\n                      =8; ALL,\n                      <jats:italic>n<\/jats:italic>\n                      =41). The ROC AUC values for the T1D GRS\n                      <jats:sub>HLA<\/jats:sub>\n                      from SNPs or HLA alleles were similar, and ranged from 0.73 (T1D GRS\n                      <jats:sub>HLA-allele-AMR<\/jats:sub>\n                      applied to FIN) to 0.88 (T1D GRS\n                      <jats:sub>HLA-allele-EUR<\/jats:sub>\n                      applied to EUR). The ROC AUC using the combined set of conditionally independent SNPs (T1D GRS\n                      <jats:sub>HLA-SNP-ALL<\/jats:sub>\n                      ) or HLA alleles (T1D GRS\n                      <jats:sub>HLA-allele-ALL<\/jats:sub>\n                      ) performed uniformly well across all ancestry groups, with values ranging from 0.82 to 0.88 for SNPs and 0.80 to 0.87 for HLA alleles.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions\/interpretation<\/jats:title>\n                    <jats:p>\n                      T1D GRS\n                      <jats:sub>HLA<\/jats:sub>\n                      models derived from SNPs performed equivalently to those derived from HLA alleles across ancestries. In addition, T1D GRS\n                      <jats:sub>HLA-SNP-ALL<\/jats:sub>\n                      and GRS\n                      <jats:sub>HLA-allele-ALL<\/jats:sub>\n                      models had consistently high ROC AUC values when applied across ancestry groups. Larger studies in more diverse populations are needed to better assess the transferability of T1D GRS\n                      <jats:sub>HLA<\/jats:sub>\n                      across ancestries.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Graphical Abstract<\/jats:title>\n                  <\/jats:sec>","DOI":"10.1007\/s00125-025-06563-8","type":"journal-article","created":{"date-parts":[[2025,10,2]],"date-time":"2025-10-02T13:10:26Z","timestamp":1759410626000},"page":"146-156","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["HLA-focused type 1 diabetes genetic risk prediction in populations of diverse ancestry"],"prefix":"10.1007","volume":"69","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0634-0319","authenticated-orcid":false,"given":"Dominika A.","family":"Michalek","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5029-595X","authenticated-orcid":false,"given":"Courtney","family":"Tern","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1120-1786","authenticated-orcid":false,"given":"Catherine C.","family":"Robertson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2643-2333","authenticated-orcid":false,"given":"Wei-Min","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6563-8334","authenticated-orcid":false,"given":"Suna","family":"Onengut-Gumuscu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3872-7793","authenticated-orcid":false,"given":"Stephen S.","family":"Rich","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,10,2]]},"reference":[{"issue":"3","key":"6563_CR1","doi-asserted-by":"publisher","first-page":"98","DOI":"10.1016\/S1525-1578(10)60658-7","volume":"3","author":"TM Williams","year":"2001","unstructured":"Williams TM (2001) Human leukocyte antigen gene polymorphism and the histocompatibility laboratory. 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Helmsley Charitable Trust (grant number 2204-05134), and grants from the JDRF, now known as Breakthrough T1D (grant numbers 1-2001-916 and 9-2011-530).","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Funding"}},{"value":"SSR has received consulting and lecture fees from Sanofi. The University of Virginia has received research support for SSR from Sanofi and from the Leona M. and Harry B. Helmsley Charitable Trust. The remaining authors declare that there are no relationships or activities that might bias, or be perceived to bias, their work.","order":5,"name":"Ethics","group":{"name":"EthicsHeading","label":"Authors\u2019 relationships and activities"}},{"value":"SSR and SO-G conceptualised, designed the study and contributed to data acquisition. DAM, CT, CCR and W-MC conducted statistical analysis. DAM, W-MC, SSR and SO-G were involved in data interpretation. DAM, SSR and SO-G drafted the manuscript. All authors contributed to the editing and critical revision of the manuscript. All authors read and approved the final version to be published. SSR is responsible for the integrity of the work as a whole.","order":6,"name":"Ethics","group":{"name":"EthicsHeading","label":"Contribution statement"}}]}}