ArticleJournal for immunotherapy of cancer2025
Macrophages expressing chimeric cytokine receptors have an inflammatory phenotype and antitumoral activity upon IL-10 or TGFβ stimulation.
Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Chimeric antigen receptor-macrophages: A new paradigm for cell therapy.Bioengineering & translational medicine · 2026Review
- ANXA2-mediated Phagocytosis Generates ARAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Engineering a PD-L1-sensing synthetic receptor for programmable macrophage response.Journal of biological engineering · 2026Article
- Interferon-induced protein IFIT3 as a molecular nexus of neuroinflammation in Alzheimer's disease and HIV-associated neurocognitive disorders.Journal of neuroinflammation · 2026Article
- The "Cold Tumor" to "Hot Tumor" transformation strategy for triple-negative breast cancer: from mechanism to clinical translation.Molecular and cellular biochemistry · 2026Review
- Secretogranin II serves as a potential prognostic biomarker and correlates with the immune microenvironment in pancreatic neuroendocrine tumors.Translational cancer research · 2026Article
- Targeting lineage-specific heterogeneity and hypovascular-fibrotic barriers may enable precision immunotherapy in pituitary neuroendocrine tumors.Frontiers in immunology · 2026Review
- Analysis of single-cell and spatial transcriptomics in TNBC cell-cell interactions.Frontiers in immunology · 2025Review
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6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundTriple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer that lacks hormone receptors and human epidermal growth factor receptor 2 (HER2) amplification, making it unresponsive to standard hormone or HER2-targeted therapies. Although immune checkpoint inhibitors (ICIs) have shown promise in tumors with high lymphocyte infiltration, their efficacy remains limited in tumors with minimal lymphocyte infiltration. Inflammatory macrophages are associated with better prognosis and response to ICIs. The tumor microenvironment (TME), however, is rich in interleukin (IL)-10 and transforming growth factor β (TGF β) inducing immunosuppressive, protumoral macrophages. Therefore, we engineer macrophages with a chimeric cytokine receptor (ChCR), designed to bind IL-10 or TGFβ and promote the generation of inflammatory and antitumoral active macrophages. Such genetically modified macrophages could be used as adoptive cell therapy (ACT).
methodsThe ChCRs consist of the extracellular domains of the IL-10 or TGFβ receptor fused to the intracellular domains of interferon (IFN)-γ receptor. Upon binding IL-10 or TGFβ, the ChCRs shall trigger STAT1 signaling, eventually rendering the macrophages pro-inflammatory. We transduced human primary macrophages with a lentiviral vector expressing the ChCR and analyzed their phenotype, secretome, and transcriptome following stimulation. Moreover, we assessed their antitumoral activity in a three-dimensional (3D) co-culture assay with TNBC spheroids.
resultsChCR macrophages showed robust STAT1 activation in response to IL-10 or TGFβ stimulation, resulting in an inflammatory phenotype similar to IFN-γ-activated macrophages, as confirmed by phenotypic markers, and transcriptomic profiling. These stimulated ChCR macrophages demonstrated significant antitumoral effects in 3D TNBC spheroids. Moreover, ChCR stimulation led to the upregulation of
conclusionWe successfully engineered macrophages to express ChCRs that induce macrophages with an inflammatory phenotype and antitumoral activity within an IL-10-rich and TGFβ-rich environment. The induction of
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