{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T22:42:22Z","timestamp":1789771342831,"version":"4.0.1"},"reference-count":100,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,1,5]],"date-time":"2026-01-05T00:00:00Z","timestamp":1767571200000},"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>\n                      HLA-G is a non-classical HLA class I molecule that promotes transplant tolerance. It engages the inhibitory receptor LILRB1 on immune effector cells, suppressing cytotoxic responses and inflammation, while promoting tolerogenic and regulatory immune phenotypes. Polymorphisms in the\n                      <jats:italic>HLA-G<\/jats:italic>\n                      3\u2032 untranslated region (3\u2032UTR) modulate HLA-G expression levels, and\n                      <jats:italic>LILRB1<\/jats:italic>\n                      promoter variants influence receptor expression. The combined effect on kidney transplant (KTx) rejection has not been systematically studied.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Living donor\u2013recipient pairs undergoing KTx were genotyped for nine variants in the\n                      <jats:italic>HLA-G<\/jats:italic>\n                      3\u2032UTR region and two single nucleotide polymorphisms (SNPs) in the\n                      <jats:italic>LILRB1<\/jats:italic>\n                      promoter (PROMO) regions. Haplotypes were arranged for both loci. Clinical endpoints were biopsy-proven T cell-mediated rejection (TCMR) within one year and antibody-mediated rejection (AMR) within five years post-transplant.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Donor positivity for\n                      <jats:italic>HLA-G<\/jats:italic>\n                      3\u2032UTR-1 or UTR-2 or negative for UTR-3 haplotype were associated with a significantly higher risk of TCMR in both univariate or multivariate analyses. Recipients lacking the\n                      <jats:italic>LILRB1<\/jats:italic>\n                      -PROMO CG haplotype also had an increased TCMR risk. The combination of an\n                      <jats:italic>HLA-G<\/jats:italic>\n                      3\u2019UTR-2 positive donor with a\n                      <jats:italic>LILRB1<\/jats:italic>\n                      -PROMO CG haplotype negative recipient was found to be an independent predictor of TCMR. In contrast, HLA-G 3\u2032UTR variants were not associated with AMR, while the presence of the recipient\n                      <jats:italic>LILRB1<\/jats:italic>\n                      -PROMO CG haplotype emerged as an independent AMR risk factor.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Donor\n                      <jats:italic>HLA-G<\/jats:italic>\n                      3\u2019UTR and recipient\n                      <jats:italic>LILRB1<\/jats:italic>\n                      -PROMO haplotypes define a functional immunogenetic axis that differentially influence TCMR and AMR. These results support the clinical potential of HLA-G\/LILRB1 genetic profiling to improve donor selection in living KTx and to guide the development of novel rejection therapies.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2025.1697839","type":"journal-article","created":{"date-parts":[[2026,1,5]],"date-time":"2026-01-05T05:30:31Z","timestamp":1767591031000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Genetic variants of the HLA-G\/LILRB1 ligand-receptor axis in donors or recipients are prognostic covariates for rejection after living kidney transplantation"],"prefix":"10.3389","volume":"16","author":[{"given":"Julian","family":"H\u00f6lzenbein","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabine","family":"Schramm","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Falko 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