{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T07:26:05Z","timestamp":1781681165222,"version":"3.54.5"},"reference-count":47,"publisher":"BMJ","issue":"2","license":[{"start":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T00:00:00Z","timestamp":1771372800000},"content-version":"unspecified","delay-in-days":17,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"name":"International Myeloma Society and Paula and Rodger Riney Foundation Translational Research Award","award":["223813.5124476.0008"],"award-info":[{"award-number":["223813.5124476.0008"]}]},{"DOI":"10.13039\/100014547","name":"Parker Institute for Cancer Immunotherapy","doi-asserted-by":"publisher","award":["C-03160"],"award-info":[{"award-number":["C-03160"]}],"id":[{"id":"10.13039\/100014547","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Dana-Farber Cancer Institute Innovation Research Fund"},{"name":"Blavatnik Therapeutics Challenge Award","award":["Grant No. 223813.5124476.0008"],"award-info":[{"award-number":["Grant No. 223813.5124476.0008"]}]},{"name":"DFCI-MIT Koch Bridge award","award":["N\/A"],"award-info":[{"award-number":["N\/A"]}]},{"name":"National Institute of Health","award":["NIH-DP2HL168562"],"award-info":[{"award-number":["NIH-DP2HL168562"]}]},{"name":"Blood Cancers United Clinical Scholar Grant","award":["N\/A"],"award-info":[{"award-number":["N\/A"]}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["1R01AI165666"],"award-info":[{"award-number":["1R01AI165666"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["J Immunother Cancer"],"accepted":{"date-parts":[[2025,12,12]]},"published-print":{"date-parts":[[2026,2]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Limited durability of clinical responses remains a major challenge in chimeric antigen receptor (CAR)-T therapy. CAR-enhancers (CAR-Es), which fuse tumor antigens to interleukin (IL)-2 muteins, provide a targeted strategy to enhance CAR-T persistence and function. It remained unclear whether CAR-Es are effective across distinct tumor contexts, when using patient-derived T cells, or in preventing exhaustion and sustaining persistence. It was also unknown whether CAR-Es can selectively expand CAR-Ts in humanized mice with pre-existing T cells, and to what extent their efficacy depends on IL-2R\u03b2\u03b3 vs IL-2R\u03b1 engagement. While IL-2R\u03b1 (CD25) has been classically linked to potent antitumor responses and memory formation, it also drives IL-2-associated toxicities, including vascular leak and preferential regulatory T cell expansion.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We systematically dissected CAR-E signaling requirements by engineering IL-2 variants with selective receptor affinities. Multiple CAR-E constructs were developed and tested across a range of in vitro and in vivo models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>We demonstrate that CAR-E activity is entirely independent of IL-2R\u03b1 and critically dependent on IL-2R\u03b2\u03b3 signaling. A next-generation IL-2R\u03b1-sparing CAR-E maintained full potency, driving robust CAR-T expansion, persistence, and tumor clearance, even at low doses and when using CAR-T cells derived from previously treated multiple myeloma patients. These CAR-T cells not only resisted exhaustion but also re-expanded months later to eradicate tumor rechallenges. In humanized mice with pre-established T cells, CAR-Es selectively expanded CAR-Ts to dominate the circulating T-cell pool. CAR-E exerted a dominant influence on CAR-T fate, overriding tumor-derived cues and enforcing consistent phenotypes across diverse preclinical models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These findings nominate a lead B-cell maturation antigen (BCMA)\u2013IL-2 CAR-E candidate with strong translational potential for clinical development and establish IL-2R\u03b2\u03b3 as a key driver of CAR-E activity. The results also identify IL-2R\u03b1 as dispensable and provide a mechanistic framework for designing safer, IL-2R\u03b1-sparing CAR-Es.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jitc-2025-013665","type":"journal-article","created":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T15:20:14Z","timestamp":1771428014000},"page":"e013665","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["Antigen\u2013IL-2 CAR-enhancer drives CAR-T fate and stemness, enhancing antitumor efficacy across models independent of IL-2R\u03b1"],"prefix":"10.1136","volume":"14","author":[{"given":"Heydar","family":"Moravej","sequence":"first","affiliation":[{"name":"Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Taha","family":"Rakhshandehroo","sequence":"additional","affiliation":[{"name":"Department of 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R","family":"Mantri","sequence":"additional","affiliation":[{"name":"Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pegah","family":"Taklifi","sequence":"additional","affiliation":[{"name":"Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Uk-Jae","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-8171-0844","authenticated-orcid":false,"given":"Benjamin B V","family":"Louis","sequence":"additional","affiliation":[{"name":"Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, Massachusetts, 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