{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T14:06:04Z","timestamp":1789049164804,"version":"build-2803163510"},"reference-count":76,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,5]],"date-time":"2026-05-05T00:00:00Z","timestamp":1777939200000},"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:p>STAT3 signaling is fundamental to T cells, where it underlies basic cellular processes like metabolism and apoptosis, as well as specialized processes like effector differentiation and cytokine production. However, mutations of STAT3 are strikingly prevalent in T-cell cancers, and aberrant or excessive STAT3 signaling is thought to mobilize cellular pathways that encourage malignancy. To better understand how STAT3 mutations drive T-cell cancers, we compared two frequent cancer-associated variants, Y640F and N647I, at the cellular and molecular levels. Using a retrogenic system, we demonstrate that they are qualitatively similar yet quantitatively distinct; each bears a gain-of-function phenotype, but Y640F has greater transcriptome-wide effects. We also discovered that these and other common STAT3 mutants invoke a T regulatory 1 (Tr1) gene program characterized by expression of IL-10 and other factors that dampen T-cell responses, including LAG3 and CD39. Importantly, \u201cTr1 skewing\u201d is evident in both mouse T cells expressing cancer-associated STAT3 variants and humans afflicted with T-cell malignancies. These studies advance current understanding of how cancer-associated mutations impact STAT3 function and reveal anti-inflammatory properties that may help transformed T cells persist, expand, and\/or avoid eradication.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1726565","type":"journal-article","created":{"date-parts":[[2026,5,5]],"date-time":"2026-05-05T05:31:37Z","timestamp":1777959097000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["T-cell lymphoma-associated STAT3 variants impose a type 1 regulatory-like phenotype"],"prefix":"10.3389","volume":"17","author":[{"given":"Aaron B.","family":"Schultz","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Miller School of Medicine, University of Miami","place":["Miami, FL, United States"]},{"name":"Sylvester Comprehensive Cancer Center, University of Miami","place":["Miami, FL, United 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