ArticleCellular & molecular immunology2024
Unsynchronized butyrophilin molecules dictate cancer cell evasion of Vγ9Vδ2 T-cell killing.
Article in Cellular & molecular immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- γδ T cells in colorectal and liver cancer.Nature reviews. Gastroenterology & hepatology · 2026Review
- Phosphoantigen-driven dissociation of butyrophilin oligomers activates γδ T cells.Cell discovery · 2026Article
- A powerful representation learning method for enhanced analysis of incomplete multi-omics data.NPJ systems biology and applications · 2026Article
- Harnessing the potential of γδ T cells through engineering and combination treatment for cancer therapies.Nature communications · 2026Review
- The integrated analysis of PRDX3 in lung cancer: biomarker potential and therapeutic target prospects.Respiratory research · 2026Article
- Proteome-wide Mendelian randomization identifies protein associations and therapeutic targets for B-cell malignancy.Blood neoplasia · 2026Article
- Cell stress activates γ9δ2 T cells via endogenous phosphoantigens and butyrophilin complex dynamics.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Shared immune perturbations in hepatocellular carcinoma-depression comorbidity and synergistic immunotherapeutic effects of fluoxetine combined with anti-PD-1.Frontiers in immunology · 2026Article
- Immunomodulatory functions of glutaminyl cyclases QPCTL and QPCT.Frontiers in immunology · 2026Review
- Integrative single-cell transcriptomics and mendelian randomization identifies BTN3A2 as a shared protective factor in Behçet's disease and inflammatory bowel disease.Frontiers in immunology · 2026Article
- Pyroglutamation of cell surface proteins CD47 and TRP1 by glutaminyl cyclase modulates therapeutic antibody binding.Communications biology · 2025Article
- Butyrophilin 3A1 Contributes to Inflammation and Induces a Lupus-Like Disease by Inhibiting the IL-38-Ferroptosis Axis.MedComm · 2025Article
- Disrupting the balance between activating and inhibitory receptors of γδT cells for effective cancer immunotherapy.Nature reviews. Cancer · 2025Review
- Central memory-enriched Vγ9Vδ2 γδ T cells via TGF-β expansion demonstrate enhancedFrontiers in immunology · 2025Article
- Fungi and cancer: unveiling the complex role of fungal infections in tumor biology and therapeutic resistance.Frontiers in cellular and infection microbiology · 2025Review
- Progress of research on γδ T cells in colorectal cancer (Review).Oncology reports · 2024Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Vγ9Vδ2 T cells are specialized effector cells that have gained prominence as immunotherapy agents due to their ability to target and kill cells with altered pyrophosphate metabolites. In our effort to understand how cancer cells evade the cell-killing activity of Vγ9Vδ2 T cells, we performed a comprehensive genome-scale CRISPR screening of cancer cells. We found that four molecules belonging to the butyrophilin (BTN) family, specifically BTN2A1, BTN3A1, BTN3A2, and BTN3A3, are critically important and play unique, nonoverlapping roles in facilitating the destruction of cancer cells by primary Vγ9Vδ2 T cells. The coordinated function of these BTN molecules was driven by synchronized gene expression, which was regulated by IFN-γ signaling and the RFX complex. Additionally, an enzyme called QPCTL was shown to play a key role in modifying the N-terminal glutamine of these BTN proteins and was found to be a crucial factor in Vγ9Vδ2 T cell killing of cancer cells. Through our research, we offer a detailed overview of the functional genomic mechanisms that underlie how cancer cells escape Vγ9Vδ2 T cells. Moreover, our findings shed light on the importance of the harmonized expression and function of gene family members in modulating T-cell activity.
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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.