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Alliance"],"accepted":{"date-parts":[[2026,7,2]]},"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:p>\n                    The genome organizer special AT-rich sequence binding protein 1 (SATB1) is critical for the development of T lymphocyte subsets by regulating\n                    <jats:italic>Foxp3<\/jats:italic>\n                    and\n                    <jats:italic>Pdcd1<\/jats:italic>\n                    expression. However, its physiological role in mature peripheral T cells has remained obscured by the severe developmental defects caused by early-stage gene knockout models. Here, we used a\n                    <jats:italic>Thpok-cre<\/jats:italic>\n                    driver to specifically delete\n                    <jats:italic>Satb1<\/jats:italic>\n                    after CD4 lineage commitment. We demonstrate that SATB1 is continuously required to suppress\n                    <jats:italic>Foxp3<\/jats:italic>\n                    expression in conventional CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells; however, this aberrant derepression does not confer Treg suppressive activity. In contrast, FoxP3\n                    <jats:sup>+<\/jats:sup>\n                    CD25\n                    <jats:sup>+<\/jats:sup>\n                    Tregs isolated from SATB1-deficient mice exhibit functional defects in immune suppressive function. Although SATB1 deletion does not cause severe global defects in the Treg transcriptome, it disrupts essential FoxP3-mediated gene regulation, resulting in a targeted failure to silence transcripts detrimental to Treg fitness. Physiologically, this Treg-specific functional defect significantly enhances antitumor immunity in a melanoma model. Our findings reveal a dual requirement for SATB1, preserving lineage fidelity by repressing\n                    <jats:italic>Foxp3<\/jats:italic>\n                    in conventional T cells, while enforcing foundational programming required for Treg suppressive function.\n                  <\/jats:p>","DOI":"10.26508\/lsa.202603763","type":"journal-article","created":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T17:35:18Z","timestamp":1784050518000},"page":"e202603763","update-policy":"https:\/\/doi.org\/10.26508\/lsa.crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["SATB1 preserves CD4\n                    <sup>+<\/sup>\n                    T-cell fidelity and establishes Treg function in antitumor immunity"],"prefix":"10.26508","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6279-166X","authenticated-orcid":true,"given":"Wooseok","family":"Seo","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02kpeqv85","id-type":"ROR","asserted-by":"publisher"}],"name":"Division of Cancer Immune Multicellular System Regulation, Center for Cancer Immunotherapy and Immunobiology (CCII), Kyoto University Graduate School of Medicine","place":[", Kyoto, Japan"]},{"name":"Department of Immunology, Nagoya University Graduate School of Medicine, Nagoya, Japan"},{"id":[{"id":"https:\/\/ror.org\/04mb6s476","id-type":"ROR","asserted-by":"publisher"}],"name":"Laboratory for Transcriptional Regulation, RIKEN Center for Integrative Medical Sciences (IMS)","place":[", Yokohama, 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