{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T19:44:18Z","timestamp":1789501458314,"version":"build-2803163510"},"reference-count":53,"publisher":"BMJ","issue":"3","license":[{"start":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T00:00:00Z","timestamp":1773014400000},"content-version":"unspecified","delay-in-days":8,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"name":"New Quality Clinical Specialty Program of High-end Medical Disciplinary Construction","award":["2024-PWXZ-08"],"award-info":[{"award-number":["2024-PWXZ-08"]}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82170200"],"award-info":[{"award-number":["82170200"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82202152"],"award-info":[{"award-number":["82202152"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82270216"],"award-info":[{"award-number":["82270216"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82300225"],"award-info":[{"award-number":["82300225"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82350101"],"award-info":[{"award-number":["82350101"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["J Immunother Cancer"],"accepted":{"date-parts":[[2026,2,15]]},"published-print":{"date-parts":[[2026,3]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Antigen escape is one of the leading causes of relapse following chimeric antigen receptor (CAR)-T therapy, particularly in multiple myeloma. A critical gap persists in understanding the tumor-intrinsic pathways that trigger antigen loss, insight essential for devising strategies to resensitize tumors to immune attack. We identify a previously uncharacterized post-translational mechanism centered on the metabolic enzyme ribonucleotide reductase subunit M2 (RRM2), termed trafficking-mediated antigen escape, to enhance cellular therapy efficacy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We combined single-cell RNA sequencing analysis with multiplex immunofluorescence to identify a clinically relevant RRM2\n                      <jats:sup>+<\/jats:sup>\n                      myeloma subpopulation exhibiting low MICA\/B abundance. Functional validation included induced pluripotent stem cell-derived myeloma organoids monitored by real-time imaging and disseminated xenograft models to assess the effect of subtoxic osalmid treatment on NKG2D CAR-T cell activity. Co-immunoprecipitation, guanosine 5\u2032-triphosphate pulldown, and confocal microscopy were used to investigate the underlying trafficking mechanism.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Single-cell analysis uncovered a clinically prevalent RRM2\n                      <jats:sup>+<\/jats:sup>\n                      myeloma subpopulation with profoundly reduced MICA\/B surface abundance, which established tumor-intrinsic heterogeneity as one of fundamental causes of NKG2D CAR-T resistance. We further demonstrated RRM2\u2019s non-canonical role as a trafficking regulator that actively shuttles MICA\/B toward lysosomal degradation via RAB7A activation while simultaneously blocking RAB11-mediated recycling. Therapeutic intervention using subtoxic osalmid, a clinically approved drug and previously characterized as an RRM2 inhibitor, successfully reversed this trafficking defect, restored MICA\/B membrane presentation and synergized with NKG2D CAR-T cells to enhance their expansion, polyfunctional cytokine secretion, and stem-like properties. This combination strategy achieved durable tumor remission in vivo by sustaining T-cell fitness while reducing exhaustion, offering an immediately actionable solution to clinical antigen escape.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our study establishes RRM2-driven trafficking as a novel and targetable mechanism of antigen escape in CAR-T therapy. By repurposing osalmid to restore MICA\/B surface presentation, we provide a clinically translatable strategy that specifically potentiates NKG2D CAR-T cell efficacy in multiple myeloma and could potentially enhance the efficacy of CAR-T across diverse antigens. This work highlights the therapeutic potential of modulating intracellular trafficking to overcome resistance in cellular immunotherapy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jitc-2025-014040","type":"journal-article","created":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T14:40:25Z","timestamp":1773067225000},"page":"e014040","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["Targeting endosomal trafficking-mediated antigen escape to resensitize myeloma to CAR-T therapy"],"prefix":"10.1136","volume":"14","author":[{"given":"Zhuning","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Hematology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guanli","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Hematology, Shanghai East Hospital, Tongji 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