{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"medRxiv"}],"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T11:53:10Z","timestamp":1791028390964,"version":"4.1.0"},"posted":{"date-parts":[[2026,9,29]]},"group-title":"Oncology","reference-count":52,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T00:00:00Z","timestamp":1790640000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.medrxiv.org\/about\/FAQ#license"}],"funder":[{"id":[{"id":"https:\/\/ror.org\/00826gz80","id-type":"ROR","asserted-by":"publisher"}]},{"id":[{"id":"https:\/\/ror.org\/03v7rwj71","id-type":"ROR","asserted-by":"publisher"}]},{"id":[{"id":"https:\/\/ror.org\/03zcxha54","id-type":"ROR","asserted-by":"publisher"}]},{"name":"Deutsche Stiftung Krebshilfe"},{"id":[{"id":"https:\/\/ror.org\/02t2ah669","id-type":"ROR","asserted-by":"publisher"}]},{"id":[{"id":"https:\/\/ror.org\/018mejw64","id-type":"ROR","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,9,29]]},"abstract":"<jats:title>Summary<\/jats:title>\n                <jats:p>Bispecific T cell engagers (BTCEs) have transformed the treatment of B cell malignancies, but how they remodel non-conventional T cell circuits in patients, and how they should be ideally combined with existing treatment backbones, remains unclear.<\/jats:p>\n                <jats:p>\n                  Here we show that CD3-engaging BTCEs convert human FOXP3\u207a regulatory T cells (Tregs) into an AP-1-imprinted hybrid cytotoxic state that contributes to tumor clearance. Leveraging longitudinal bone marrow and peripheral blood sampling from patients with newly diagnosed multiple myeloma (NDMM) treated with BTCE-based induction in the phase 2 (GMMG-HD10\/DSMM-XX\/MajesTEC-5) trial, which achieves uniformly deep, minimal residual disease (MRD)-negative remissions, we integrate single-cell RNA, ATAC and TCR sequencing with functional and metabolic profiling to define the underlying mechanism. BTCE-containing induction drives expansion of cytotoxic CD8\u207a clones and the emergence of a Treg population characterized by GZMA, GNLY and NKG7 expression, enriched cytotoxic gene signatures, and licensed by BATF-AP-1-centered chromatin remodeling.\n                  <jats:italic>In vitro<\/jats:italic>\n                  , BTCE-exposed Tregs acquire\n                  <jats:italic>bona fide<\/jats:italic>\n                  lytic function, killing tumor cells in a target- and dose-dependent manner and undergoing metabolic rewiring towards an effector-like state while retaining canonical Treg lineage markers. Immunomodulatory drugs (IMiDs) do not initiate but quantitatively amplify and qualitatively reshape this BTCE-driven cytotoxic program, providing a mechanistic rationale for BTCE-IMiD combination regimens. Cytotoxic Treg reprogramming is conserved across BTCEs targeting BCMA, GPRC5D, and CD19 and across multiple myeloma, as well as acute lymphoblastic leukemia.\n                <\/jats:p>\n                <jats:p>These findings reveal unexpected plasticity of human Tregs under synthetic T cell engagement and establish cytotoxic Tregs as active effectors, candidate biomarkers and tractable levers for optimizing T cell-redirecting immunotherapy.<\/jats:p>\n                <jats:sec>\n                  <jats:title>Highlights<\/jats:title>\n                  <jats:list list-type=\"bullet\">\n                    <jats:list-item>\n                      <jats:p>Frontline teclistamab (BCMA\u00d7CD3) induces deep MRD-negative remissions in newly diagnosed multiple myeloma patients and reshapes the T cell compartment in the phase 2 MajesTEC-5 trial.<\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>\n                        BTCEs convert FOXP3\u207a Tregs into AP-1-imprinted cytotoxic effector cells\n                        <jats:italic>in vivo<\/jats:italic>\n                        .\n                      <\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>IMiDs amplify BTCE-driven cytotoxic Treg reprogramming without loss of identity.<\/jats:p>\n                    <\/jats:list-item>\n                    <jats:list-item>\n                      <jats:p>Cytotoxic reprogramming of Tregs is observed across BTCEs and blood cancers.<\/jats:p>\n                    <\/jats:list-item>\n                  <\/jats:list>\n                <\/jats:sec>","DOI":"10.64898\/2026.09.23.26363285","type":"posted-content","created":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T22:55:12Z","timestamp":1790722512000},"source":"Crossref","is-referenced-by-count":0,"title":["CD3-engaging bispecific antibodies convert human regulatory T cells into cytotoxic effectors"],"prefix":"10.64898","author":[{"given":"Julius J.","family":"Michel","sequence":"first","affiliation":[{"name":"German Cancer Research Center (DKFZ), JRG Hematology and Immune Engineering, Heidelberg, Germany"},{"name":"German Cancer Consortium (DKTK), Core Center Heidelberg, Heidelberg, Germany"},{"name":"Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH), Heidelberg, Germany"},{"name":"Medical Faculty Heidelberg, Heidelberg University and Heidelberg Myeloma Center, Department of Hematology, Oncology and Rheumatology, Heidelberg University Hospital, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan H.","family":"Frenking","sequence":"additional","affiliation":[{"name":"Medical Faculty Heidelberg, Heidelberg University and Heidelberg Myeloma Center, Department of Hematology, Oncology and Rheumatology, Heidelberg University Hospital, Heidelberg, Germany"},{"name":"German Cancer Research Center 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