{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T05:11:17Z","timestamp":1778217077605,"version":"3.51.4"},"reference-count":60,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T00:00:00Z","timestamp":1778198400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Genome-wide association studies have implicated the human leukocyte antigen\/major histocompatibility complex (HLA\/MHC) region in amyotrophic lateral sclerosis (ALS) susceptibility, and immune dysregulation is increasingly recognised as a modifier of disease course. High-resolution HLA data for ALS remain confined to European and East Asian ancestries. We tested whether classical HLA class I and class II variation contributes to ALS susceptibility in a Kuwaiti cohort.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We analysed 38 unrelated ALS cases (mean age, 57.4 years; 63.2% male) and 150 population-matched controls (mean age, 57.0 years) from Kuwait. HLA-A, -B, -C, -DRB1, -DQA1, and -DQB1 alleles were typed at two-field resolution using HLA-HD from next-generation sequencing (NGS) data. Allele, haplotype, and amino-acid residue associations were tested in BIGDAWG with locus-specific Bonferroni correction, with additional across-locus sensitivity analysis. Significant class II residues were mapped onto AlphaFold 3 structural models and interpreted alongside published class II crystal structures.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      No class I allele, haplotype, or residue remained significant after correction. In class II, DQA1*02:01 [odds ratio (OR) = 3.18, 95% confidence interval (CI) 1.67 to 5.95,\n                      <jats:italic>p<\/jats:italic>\n                      <jats:sub>c<\/jats:sub>\n                      = 0.0007], DRB1*07:01 (OR\u00a0=\u00a03.00, 95% CI: 1.58\u20135.59,\n                      <jats:italic>p<\/jats:italic>\n                      <jats:sub>c<\/jats:sub>\n                      = 0.001), and DQB1*02:02 (OR\u00a0=\u00a02.48, 95% CI: 1.28\u20134.69,\n                      <jats:italic>p<\/jats:italic>\n                      <jats:sub>c<\/jats:sub>\n                      = 0.03) were enriched in cases. The extended haplotype DQA1*02:01~DQB1*02:02~DRB1*07:01 (DR7\u2013DQ2.2) conferred increased odds of ALS (OR\u00a0=\u00a03.11, 95% CI: 1.53\u20136.19,\n                      <jats:italic>p<\/jats:italic>\n                      <jats:sub>c<\/jats:sub>\n                      = 0.002). Amino-acid residue analysis identified convergent risk positions in DQ\u03b11 (positions 47, 52, and 54; OR\u00a0=\u00a03.18,\n                      <jats:italic>p<\/jats:italic>\n                      <jats:sub>c<\/jats:sub>\n                      = 0.006) and DR\u03b21 (positions 11, 13, 14, 25, and 30; OR\u00a0=\u00a02.84,\n                      <jats:italic>p<\/jats:italic>\n                      <jats:sub>c<\/jats:sub>\n                      = 0.03) that map to the peptide-binding groove and correspond to the defining motifs of DQA1*02:01 and DRB1*07:01.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Using high-resolution NGS-based HLA typing in a Kuwaiti cohort, we identified a class II risk signal for ALS centred on the DR7\u2013DQ2.2 haplotype with convergent residue-level support in the peptide-binding domains. These findings support a contribution of class II-restricted antigen presentation to ALS susceptibility and warrant functional validation and replication in larger, independent Middle Eastern cohorts.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1820694","type":"journal-article","created":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T04:48:27Z","timestamp":1778215707000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Classical HLA class II associations with ALS in Kuwait reveal a DR7\u2013DQ2.2 risk haplotype"],"prefix":"10.3389","volume":"17","author":[{"given":"Mohammed","family":"Dashti","sequence":"first","affiliation":[{"name":"Translational Research Department, Dasman Diabetes Institute","place":["Kuwait City, Kuwait"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Faye","family":"AlAbdulghafour","sequence":"additional","affiliation":[{"name":"Department of Neurology, Kuwait Institute of Medical Specializations, Kuwait Ministry of Health","place":["Kuwait City, Kuwait"]},{"name":"Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King\u2019s College London","place":["London, United Kingdom"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ohood","family":"AlMutairi","sequence":"additional","affiliation":[{"name":"Department of Neurology, Kuwait Institute of Medical Specializations, Kuwait Ministry of Health","place":["Kuwait City, Kuwait"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anwar","family":"Mohammad","sequence":"additional","affiliation":[{"name":"Translational Research Department, Dasman Diabetes Institute","place":["Kuwait City, Kuwait"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Md Zubbair","family":"Malik","sequence":"additional","affiliation":[{"name":"Translational Research Department, Dasman Diabetes 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