ArticleNature biomedical engineering2026
A trispecific antibody engaging T cells with tumour and myeloid cells augments antitumour immunity.
Article in Nature biomedical engineering, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Radiotherapy and immunotherapy in cancer treatment: mechanisms of clinical synergy.The Journal of clinical investigation · 2026Review
- The Evolving Landscape of Immune Regulation and Immunotherapy in Cholangiocarcinoma and Biliary Tract Cancer.Cancers · 2026Review
- Targeted delivery of TGF-β inhibitor via LHRH-NanoTi reverses the NAT10/ac4C-mediated cisplatin-induced immunosuppressive tumor microenvironment in ovarian cancer.Journal of nanobiotechnology · 2026Article
- Trispecific antibodies: is more always better? Advances and boundaries.Precision clinical medicine · 2026Article
- Circling back to RNA vaccines.Nature biotechnology · 2026Article
- The absence of B7-H4 inhibits PD-L1 expression by driving a methylation of PD-L1 promoter in breast cancer cells.Breast cancer research : BCR · 2026Article
- Trispecific engager overcomes tumoural immunosuppressive environment.Nature biomedical engineering · 2026Article
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Immunologically unresponsive tumours often resist immune checkpoint inhibitors due to the low abundance of tumour-specific T cells and an immunosuppressive microenvironment, despite pronounced infiltration of non-tumour-specific (bystander) T cells. Here we analysed single-cell RNA sequencing data from 300 patients across 17 tumour types, identifying abundant but functionally restrained bystander T cells in multiple malignancies, including ovarian and colorectal cancer. To enhance antitumour immunity in such contexts, we engineered B7H3xCD3xPDL1, a trispecific immunoglobulin-based T cell engager targeting B7H3, CD3 and PDL1, to redirect T cells while mitigating immunosuppression. Functional validation in co-culture systems, patient-derived tumour suspensions and fragments, and humanized mouse models showed T cell activation and tumour killing. Imaging cytometry and single-cell transcriptomics revealed IFNγ-dependent macrophage reprogramming and IL-15 secretion, establishing a feed-forward loop that augments T cell functionality. A machine learning model trained on ex vivo cytotoxicity and transcriptomic data predicted patient responsiveness, supporting data-driven clinical stratification for solid tumour immunotherapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.