{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T22:43:06Z","timestamp":1793227386020,"version":"4.5.0"},"reference-count":34,"publisher":"American Society for Clinical Investigation","issue":"2","license":[{"start":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T00:00:00Z","timestamp":1769126400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R01 DK057846"],"award-info":[{"award-number":["R01 DK057846"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["1S10OD03036301A1"],"award-info":[{"award-number":["1S10OD03036301A1"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000901","name":"Juvenile Diabetes Research Foundation International","doi-asserted-by":"crossref","award":["JDRF 2-SRA-2022-1197-S-B"],"award-info":[{"award-number":["JDRF 2-SRA-2022-1197-S-B"]}],"id":[{"id":"10.13039\/100000901","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,1,23]]},"abstract":"<jats:p>\n                    Treatment with anti-CD3 monoclonal antibody (mAb) can delay or prevent type 1 diabetes in mice and humans by modulating the immune-mediated destruction of \u03b2 cells. A single course of treatment may have lasting efficacy, but the mechanisms that account for these prolonged effects, i.e., \u201coperational tolerance,\u201d are not clear. Here, we used paired single-cell RNA and T cell receptor sequencing to characterize islet-infiltrating T cells and their counterpart in paired pancreatic lymph nodes from anti-CD3 mAb\u2013treated nonobese diabetic (NOD) mice in remission. We found that after anti-CD3 mAb treatment, T cells that infiltrate the islets are more heterogeneous and have hybrid features including characteristics of T stem cell\u2013like memory and reduced effector function compared with those from untreated prediabetic NOD mice. Autoantigen-reactive CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells persist after treatment, but they also show features of stemness and reduced pathogenicity. Our findings describe the reshaping of islet-infiltrating and autoreactive T cells and \u03b2 cells that lead to operational, but tenuous, tolerance to autoimmune diabetes following anti-CD3 mAb treatment.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.192755","type":"journal-article","created":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T19:00:43Z","timestamp":1769108443000},"source":"Crossref","is-referenced-by-count":5,"title":["Anti-CD3 mAb treatment reshapes infiltrating T and \u03b2 cells in the islets in autoimmune diabetes"],"prefix":"10.1172","volume":"11","author":[{"given":"Ying","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Immunobiology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maxwell","family":"Spurrell","sequence":"additional","affiliation":[{"name":"Department of 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