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However, how differences in affinity and specificity may support Treg function compared with autoimmune T cell function remains unresolved. In this study, we analyzed the T cell receptor (TCR) repertoires of the regulatory and effector T cells that spontaneously infiltrate pancreatic islets of nonobese diabetic mice and therefore share antigen specificity. Using 2-dimensional micropipette measurements of TCR affinity, we show that effector and regulatory T cell-derived TCRs possess similar wide-ranging affinities for self-antigen. Treg-derived TCRs conferred variable protective function and Treg suppressive capacity was, in part, determined by the relative antigen-reactivity of effector T cells. Interestingly, when expressing the same TCR, Tregs showed higher Nur77-GFP expression than effector T cells in vivo, suggesting a Treg-intrinsic ability to compete for antigen. In vitro, we observed accelerated Treg TCR activation, suggesting that Tregs are poised for faster response to antigen than T effectors. Our findings expose a subpopulation of Tregs possessing low-affinity, suboptimal TCRs, obscured by apparent higher Nur77 expression in Tregs as a whole.<\/jats:p>","DOI":"10.1093\/jimmun\/vkag136","type":"journal-article","created":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T17:05:28Z","timestamp":1783011928000},"source":"Crossref","is-referenced-by-count":0,"title":["Increased Nur77 is disconnected from TCR affinity in insulin-specific Tregs"],"prefix":"10.1093","volume":"215","author":[{"given":"Yi","family":"Jing","sequence":"first","affiliation":[{"name":"Department of Pathology, Division of Microbiology and Immunology, University of Utah , Salt Lake City, UT,","place":["United States"]},{"name":"Section of Diabetes and Endocrinology, Department of Pediatrics, Texas Children\u2019s Hospital, Baylor College of Medicine , Houston, TX,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuelin","family":"Kong","sequence":"additional","affiliation":[{"name":"Section of Diabetes and Endocrinology, Department of Pediatrics, Texas Children\u2019s Hospital, Baylor College of Medicine , Houston, TX,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Baoyu","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Pathology, Division of Microbiology and Immunology, University of Utah , Salt Lake City, UT,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth","family":"Kolawole","sequence":"additional","affiliation":[{"name":"Department of Pathology, Division of Microbiology and Immunology, University of Utah , Salt Lake City, UT,","place":["United 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Endocrinology, Department of Pediatrics, Texas Children\u2019s Hospital, Baylor College of Medicine , Houston, TX,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian D","family":"Evavold","sequence":"additional","affiliation":[{"name":"Department of Pathology, Division of Microbiology and Immunology, University of Utah , Salt Lake City, UT,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew L","family":"Bettini","sequence":"additional","affiliation":[{"name":"Department of Pathology, Division of Microbiology and Immunology, University of Utah , Salt Lake City, UT,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Bettini","sequence":"additional","affiliation":[{"name":"Department of Pathology, Division of Microbiology and Immunology, University of Utah , Salt Lake City, UT,","place":["United 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