ArticleMolecular therapy : the journal of the American Society of Gene Therapy2025
CAR-mediated target recognition limits TCR-mediated target recognition of TCR- and CAR-dual-receptor-edited T cells.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- The T Cell Receptor: Molecular Sensor, Therapeutic Mediator and Probabilistic Driver of Adaptive Immunity.Immunological reviews · 2026Review
- Advances in targeted and cellular therapies for relapsed/refractory mantle cell lymphoma: immunotherapeutic strategies and challenges.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Cre-dependent gene expression enables thymic development of autoreactive tumor-associated antigen targeting CAR-T cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- T-cell receptor therapy in ovarian cancer: concepts and challenges.Journal of ovarian research · 2025Review
- Multiplex engineering and multifunction T cells for precise and effective immunotherapies.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
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Abstract
Antigen escape can compromise the efficacy of chimeric antigen receptor- (CAR-) or T cell receptor- (TCR-) engineered T cells. Targeting multiple antigens can effectively limit antigen escape, and combining CAR-with TCR-mediated targeting can significantly broaden the spectrum of targetable antigens. Here, we explored whether dual-antigen specificity can be installed on T cells using combined TCR and CAR engineering to prevent antigen escape of multiple myeloma (MM). We report the generation of CD8 T cells that were transduced to express a transgenic TCR, targeting a peptide derived from transcriptional coactivator BOB1 in the context of HLA-B∗07:02, alongside a BCMA-targeting CAR. Those T cells, called TRaCR T cells, efficiently recognized target cells that were resistant to either BOB1 TCR or BCMA CAR T cells, illustrating general dual specificity. In the presence of both antigens, however, target cell recognition was preferentially conferred via the CAR, compromising TCR-mediated target cell recognition. Importantly, this resulted in a survival advantage for tumor cells lacking expression of BCMA in an in vivo model of heterogeneous MM. In conclusion, we demonstrate general dual specificity of TRaCR T cells but advise caution when using TRaCR T cells as a strategy to target heterogeneous tumors.
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