{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T13:01:01Z","timestamp":1792242061891,"version":"4.4.0"},"reference-count":27,"publisher":"American Diabetes Association","issue":"9","license":[{"start":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T00:00:00Z","timestamp":1783382400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.diabetesjournals.org\/journals\/pages\/license"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["K12DK133995"],"award-info":[{"award-number":["K12DK133995"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Breakthrough T1D","award":["Advanced Postdoctoral Fellowship"],"award-info":[{"award-number":["Advanced Postdoctoral Fellowship"]}]}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,9,1]]},"abstract":"<jats:sec>\n                    <jats:title>OBJECTIVE<\/jats:title>\n                    <jats:p>Posttransplant type 1 diabetes (T1D) is typically attributed to transferred donor autoimmunity. We investigated a distinct etiology in a patient who developed diabetes following haploidentical hematopoietic cell transplantation, assessing whether autoimmunity originated from donor or residual host cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESEARCH DESIGN AND METHODS<\/jats:title>\n                    <jats:p>Leveraging HLA disparity between the haploidentical donor and recipient, we used HLA class II tetramers to enumerate islet-specific CD4+ T cells in peripheral blood restricted by shared versus recipient-only HLA alleles.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>Tetramer analysis revealed an expanded population of islet-specific T cells in the recipient. The donor showed no such expansion. Despite 99% donor T-cell chimerism, &amp;gt;80% of the islet-specific T cells were restricted by recipient-unique HLA alleles, suggesting they originated from the residual host fraction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS<\/jats:title>\n                    <jats:p>T1D in this patient was most likely driven by residual recipient-derived T cells. Their survival despite myeloablative conditioning and repeated immunotherapy underscores the remarkable durability of established islet autoimmunity.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2337\/dc26-0795","type":"journal-article","created":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T14:11:02Z","timestamp":1783433462000},"page":"1694-1699","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":1,"title":["Type 1 Diabetes Driven by Residual Recipient T Cells After Hematopoietic Cell Transplantation: A Case Report"],"prefix":"10.2337","volume":"49","author":[{"given":"Martin A.","family":"Thelin","sequence":"first","affiliation":[{"name":"Diabetes Center, University of California San Francisco 1 , San Francisco, CA"},{"name":"Department of Pediatrics, University of California San Francisco 2 , San Francisco, CA"},{"name":"Division of Pediatric Endocrinology, University of California San Francisco 3 , San 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