ArticleOncogene2025
Unveiling the role of TAM-derived extracellular vesicles in glioma progression through Treg polarization and immune suppression.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
5 citing papers in PubMed.
- Hypoxic Endothelial-Cell-Derived Exosomal lnc-DKK3 Reprograms Tumor-Associated Macrophages via USP47/PD-L1/RelA Axis to Promote Glioma Progression.Research (Washington, D.C.) · 2026Article
- Metabolic reprogramming and immunosenescence: a new sight for glioma therapy.Frontiers in cell and developmental biology · 2026Review
- Polarization-Specific Macrophage-Derived Extracellular Vesicles: Molecular Cargo, Tumor Microenvironment Remodeling, and Therapeutic Opportunities.International journal of nanomedicine · 2026Review
- The neuro-immuno-metabolic axis of exercise: a unified mechanistic framework for exercise-induced cognitive enhancement and psychological resilience.Frontiers in psychology · 2026Review
- Tumor-Promoting Crosstalk of MMP11⁺ Fibroblasts and SPP1⁺ Macrophages Drive Poor Prognosis in Breast Cancer: Integrated Multi-Omics Analysis.ImmunoTargets and therapy · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the context of gliomas, tumor-associated macrophages (TAMs) and regulatory T cells (Tregs) play crucial roles in shaping the tumor microenvironment (TME). This study focused on elucidating the mechanism by which TAM-derived extracellular vesicles (EVs) influence Treg differentiation and contribute to glioma progression. Through comprehensive single-cell RNA sequencing (scRNA-seq) analysis, the glioma TME was characterized by an abundance of TAMs exhibiting M2 polarization and increased Treg differentiation. Notably, TAM EVs were identified as potent inducers of Treg differentiation, with the downregulation of Bactericidal/Permeability-Increasing protein (BPI) being associated with this process. In vivo experiments utilizing a mouse model of glioma further demonstrated that TAM-derived EVs promoted glioma growth by enhancing Treg-mediated immunosuppression while dampening pro-inflammatory responses. This study highlights the critical role of TAM-derived EVs in modulating Treg differentiation and supporting glioma progression, suggesting that interventions targeting TAM EVs or regulating BPI expression could offer novel therapeutic avenues for combating immune suppression and inhibiting glioma development.
Indexed as
Identifiers
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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.