{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T16:15:40Z","timestamp":1789661740262,"version":"4.0.1"},"reference-count":75,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2024,7,10]],"date-time":"2024-07-10T00:00:00Z","timestamp":1720569600000},"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>Introduction<\/jats:title>\n                    <jats:p>\n                      Genetic predisposition to autoimmune encephalitis with antibodies against N-methyl-D-aspartate receptor (NMDAR) is poorly understood. Given the diversity of associated environmental factors (tumors, infections), we hypothesized that human leukocyte antigen (\n                      <jats:italic>HLA<\/jats:italic>\n                      ) and killer-cell immunoglobulin-like receptors (\n                      <jats:italic>KIR<\/jats:italic>\n                      ), two extremely polymorphic gene complexes key to the immune system, might be relevant for the genetic predisposition to anti-NMDAR encephalitis. Notably, KIR are chiefly expressed by Natural Killer (NK) cells, recognize distinct HLA class I allotypes and play a major role in anti-tumor and anti-infection responses.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We conducted a Genome Wide Association Study (GWAS) with subsequent control-matching using Principal Component Analysis (PCA) and\n                      <jats:italic>HLA<\/jats:italic>\n                      imputation, in a multi-ethnic cohort of anti-NMDAR encephalitis (n=479);\n                      <jats:italic>KIR<\/jats:italic>\n                      and\n                      <jats:italic>HLA<\/jats:italic>\n                      were further sequenced in a large subsample (n=323). PCA-controlled logistic regression was then conducted for carrier frequencies (\n                      <jats:italic>HLA<\/jats:italic>\n                      and\n                      <jats:italic>KIR<\/jats:italic>\n                      ) and copy number variation (\n                      <jats:italic>KIR<\/jats:italic>\n                      ). HLA-KIR interaction associations were also modeled. Additionally, single cell sequencing was conducted in peripheral blood mononuclear cells from 16 cases and 16 controls, NK cells were sorted and phenotyped.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Anti-NMDAR encephalitis showed a weak\n                      <jats:italic>HLA<\/jats:italic>\n                      association with\n                      <jats:italic>DRB1*01:01~DQA1*01:01~DQB1*05:01<\/jats:italic>\n                      (OR=1.57, 1.51, 1.45; respectively), and\n                      <jats:italic>DRB1*11:01<\/jats:italic>\n                      (OR=1.60); these effects were stronger in European descendants and in patients without an underlying ovarian teratoma. More interestingly, we found increased copy number variation of\n                      <jats:italic>KIR2DL5B<\/jats:italic>\n                      (OR=1.72), principally due to an overrepresentation of\n                      <jats:italic>KIR2DL5B*00201<\/jats:italic>\n                      . Further, we identified two allele associations in framework genes,\n                      <jats:italic>KIR2DL4*00103<\/jats:italic>\n                      (25.4% vs. 12.5% in controls, OR=1.98) and\n                      <jats:italic>KIR3DL3*00302<\/jats:italic>\n                      (5.3% vs. 1.3%, OR=4.44). Notably, the ligands of these KIR2DL4 and KIR3DL3, respectively, HLA-G and HHLA2, are known to act as immune checkpoint with immunosuppressive functions. However, we did not find differences in specific KIR-HLA ligand interactions or HLA-G polymorphisms between cases and controls. Similarly, gene expression of CD56\n                      <jats:sup>dim<\/jats:sup>\n                      or CD56\n                      <jats:sup>bright<\/jats:sup>\n                      NK cells did not differ between cases and controls.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>Our observations for the first time suggest that the HLA-KIR axis might be involved in anti-NMDAR encephalitis. While the genetic risk conferred by the identified polymorphisms appears small, a role of this axis in the pathophysiology of this disease appears highly plausible and should be analyzed in future studies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2024.1423149","type":"journal-article","created":{"date-parts":[[2024,7,10]],"date-time":"2024-07-10T00:26:36Z","timestamp":1720571196000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":17,"title":["HLA and KIR genetic association and NK cells in anti-NMDAR encephalitis"],"prefix":"10.3389","volume":"15","author":[{"given":"Vicente","family":"Peris Sempere","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guo","family":"Luo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sergio","family":"Mu\u00f1iz-Castrillo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne-Laurie","family":"Pinto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G\u00e9raldine","family":"Picard","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V\u00e9ronique","family":"Rogemond","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maarten J.","family":"Titulaer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carsten","family":"Finke","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank","family":"Leypoldt","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregor","family":"Kuhlenb\u00e4umer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"name":"GENERATE study group","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hannah F.","family":"Jones","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Russell C.","family":"Dale","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sophie","family":"Binks","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarosh R.","family":"Irani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna E.","family":"Bastiaansen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juna M.","family":"de Vries","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marienke A. 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