ArticleCommunications biology2024
CD3-engaging bispecific antibodies trigger a paracrine regulated wave of T-cell recruitment for effective tumor killing.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The trial behind it
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Who cites it
6 citing papers in PubMed.
- Cytokine release syndrome in solid tumours: mechanism-based therapeutic strategies for prevention and management.Therapeutic advances in medical oncology · 2026Review
- Review
- Article
- Bispecific antibody targeting CD155 mediates T-cell immunotherapy against human gynecological malignancies.Investigational new drugs · 2025Article
- CD3xHER2 bsAb-Mediated Activation of Resting T-cells at HER2 Positive Tumor Clusters Is Sufficient to Trigger Bystander Eradication of Distant HER2 Negative Clusters Through IFNγ and TNFα.European journal of immunology · 2025Article
- ADCC: the rock band led by therapeutic antibodies, tumor and immune cells.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The mechanism of action of bispecific antibodies (bsAbs) directing T-cell immunity to solid tumors is incompletely understood. Here, we screened a series of CD3xHER2 bsAbs using extracellular matrix (ECM) embedded breast cancer tumoroid arrays exposed to healthy donor-derived T-cells. An initial phase of random T-cell movement throughout the ECM (day 1-2), was followed by a bsAb-dependent phase of active T-cell recruitment to tumoroids (day 2-4), and tumoroid killing (day 4-6). Low affinity HER2 or CD3 arms were compensated for by increasing bsAb concentrations. Instead, a bsAb binding a membrane proximal HER2 epitope supported tumor killing whereas a bsAb binding a membrane distal epitope did not, despite similar affinities and intra-tumoroid localization of the bsAbs, and efficacy in 2D co-cultures. Initial T-cell-tumor contact through effective bsAbs triggered a wave of subsequent T-cell recruitment. This critical surge of T-cell recruitment was explained by paracrine signaling and preceded a full-scale T-cell tumor attack.
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Registered trials
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