ArticleJournal for immunotherapy of cancer2025
Arginase-1-specific T cells target and modulate tumor-associated macrophages.
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 31 papers.
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Who cites it
31 citing papers in PubMed.
- Targeting the tumor microenvironment: a new strategy for natural products in breast cancer therapy.Natural products and bioprospecting · 2026Review
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- Multi-omics analysis of arginine metabolism in ovarian cancer: A prognostic signature and GTF2F2-driven stromal remodeling.Translational oncology · 2026Article
- Leveraging Macrophage Metabolic Reprogramming for Enhanced Anti-Tumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Induction of senescence like macrophages by hepatocellular carcinoma cells in vitro.Discover oncology · 2026Article
- Review
- Immune modulatory vaccines targeting tumor microenvironment antigens: recent advances in oncology and beyond.Signal transduction and targeted therapy · 2026Review
- Multi-omics profiling identifies ADAM9 as a key efferocytosis driver in lung adenocarcinoma.Frontiers in immunology · 2026Article
- Article
- Amino Acid Metabolic Enzymes in Gastric Cancer: Roles and Mechanisms in Tumorigenesis and Progression.Oncology research · 2026Review
- Amino acid metabolic regulatory network in tumor immune escape: mechanistic exploration and intervention directions.Frontiers in immunology · 2026Review
- Immunosuppressive cells as barriers to cancer therapy: mechanisms and emerging solutions.Frontiers in immunology · 2026Review
- Single-cell dissection of hepatocellular carcinoma immunity: from heterogeneous subtypes to precision therapeutics.Frontiers in immunology · 2026Review
- Prognostic biomarkers and regulatory mechanisms associated with lysine β-hydroxybutyrylation modification in prostate cancer.Frontiers in molecular biosciences · 2026Article
- Single-cell omics reveals arg-1 as a key regulator of age-dependent macrophage-mediated cartilage repair.PloS one · 2026Article
- Macrophage plasticity in thyroid eye disease: dual effects of inflammation and fibrosis.Frontiers in immunology · 2026Review
- ARG1-polyamine axis: cell-type-specific functions in disease pathogenesis and therapeutic targeting.Frontiers in immunology · 2026Review
- Hypoxic tumor microenvironment and immune cell dynamics: From metabolic reprogramming to therapeutic innovation.Iranian journal of basic medical sciences · 2026Review
- The tumor microenvironment: a dynamic ecosystem and therapeutic nexus in modern oncology.Frontiers in pharmacology · 2026Review
- The role of deoxycholic acid in macrophage polarization and remodeling of the tumor microenvironment during colorectal adenoma-carcinoma transition.Cancer & metabolism · 2025Article
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundArginase-1 (Arg1) expressing tumor-associated macrophages (TAMs) may create an immune-suppressive tumor microenvironment (TME), which is a significant challenge for cancer immunotherapy. We previously reported the existence of Arg1-specific memory T cells among peripheral blood mononuclear cells (PBMCs) and described that Arg-1-based immune modulatory vaccines (IMVs) control tumor growth and alter the M1/M2 macrophage ratio in murine models of cancer. In the present study, we investigated how Arg1-specific T cells can directly target TAMs and influence their polarization.
methodsMurine Arg1-specific CD4+T cells isolated from splenocytes of animals vaccinated with an Arg1-derived peptide in the adjuvant montanide were co-cultured with either
resultsWe show that Arg1-based IMV-mediated tumor control was linked to a decrease in multiple immunosuppressive pathways in the TAM population of the treated animals. Tumor-conditioned media (TCM) derived from Arg1-vaccinated mice induced significantly higher upregulation of MHC-II on exposed myeloid cells compared with controls. Furthermore, murine CD4+Arg1-specific T cells were able to target TAMs and effectively reprogram their phenotype
conclusionsTAMs may be directly targeted and modulated by Arg1-specific CD4+T cells. These findings provide a strong rationale for future clinical development of Arg1-based IMVs to alter the immune-suppressive TME by reprogramming TAMs and promoting a proinflammatory TME.
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