{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T02:03:08Z","timestamp":1789437788606,"version":"build-2803163510"},"reference-count":32,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T00:00:00Z","timestamp":1788739200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T00:00:00Z","timestamp":1788739200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["P30 CA016520"],"award-info":[{"award-number":["P30 CA016520"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["P30 AI045008"],"award-info":[{"award-number":["P30 AI045008"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["KL2TR001879"],"award-info":[{"award-number":["KL2TR001879"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["1K08DK141964\u201001A1"],"award-info":[{"award-number":["1K08DK141964\u201001A1"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["1R01HL174612\u201001A1"],"award-info":[{"award-number":["1R01HL174612\u201001A1"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000005","name":"U.S. Department of Defense","doi-asserted-by":"publisher","award":["HT94252410445"],"award-info":[{"award-number":["HT94252410445"]}],"id":[{"id":"10.13039\/100000005","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. pediatr. gastroenterol. nutr."],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Activated T cell pediatric acute liver failure (TC\u2010PALF) is characterized by CD8+T cells in liver and peripheral blood. TC\u2010PALF patients are at increased risk of developing aplastic anemia (AA), an immune\u2010mediated disorder in which CD8+ T cells target hematopoietic stem and progenitor cells. Clonal expansion of T cell receptors (TCRs) and specific human leukocyte antigen (HLA) class I risk alleles have been reported in AA. We hypothesized TC\u2010PALF shares similar HLA associations and exhibits increased TCR clonality.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Thirty\u2010one TC\u2010PALF and 15 other PALF diagnosis (other\u2010PALF) patients enrolled in the Pediatric Acute Liver Failure Study Group (PALFSG) were included. Liver tissue DNA underwent TCR \u03b2\u2010chain (TCR\u03b2) complementarity\u2010determining region 3 sequencing and HLA genotyping. HLA allele frequencies were compared with ethnicity\u2010matched controls. TCR clonality was assessed and Grouping of Lymphocyte Interactions by Paratope Hotspots 2 (GLIPH2) was used to identify antigen\u2010convergent, disease\u2010associated TCR groups.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>HLA class I alleles HLA\u2010A*23:01, HLA\u2010B*35:03, HLA\u2010B*52:01, and HLA\u2010B*39:05 were significantly overrepresented among TC\u2010PALF patients compared to ethnicity\u2010matched controls. Hepatic TCR\u03b2 clonality was increased in the TC\u2010PALF group. GLIPH2 identified 158 statistically significant TCR convergence groups enriched in TC\u2010PALF with significant HLA associations, representing putative antigen\u2010specific TCR clusters.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Enrichment of specific HLA class I alleles, increased hepatic TCR clonality, and HLA\u2010associated TCR convergence groups support an HLA\u2010restricted, antigen\u2010driven CD8+ T cell response as a central mechanism of TC\u2010PALF. These findings provide a mechanistic framework for antigen discovery and future development of immunogenetic biomarkers to improve disease classification, risk stratification, and targeted immunomodulatory therapy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/jpn3.70573","type":"journal-article","created":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T09:21:08Z","timestamp":1788772868000},"source":"Crossref","is-referenced-by-count":0,"title":["Identification of human leukocyte antigen class I risk alleles and enriched T cell receptor groups in activated T cell pediatric acute liver failure"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3339-9372","authenticated-orcid":false,"given":"Catherine A.","family":"Chapin","sequence":"first","affiliation":[{"name":"Division of Gastroenterology, Hepatology and Nutrition, Ann &amp; Robert H. 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