ArticleFrontiers in immunology2026
TREM1 unleashes immunosuppression in glioma: targeting macrophage polarization as a new therapeutic vulnerability.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Tumor-associated macrophages (TAMs) represent the predominant immune cell subset within the glioma tumor microenvironment (TME). This study aims to investigate the clinical significance of TAM-related TREM1 in glioma and its potential mechanism in promoting malignant progression. Methods: Bioinformatics analyses were employed to assess the expression pattern and prognostic value of TREM1 in glioma. Single-cell sequencing, immunohistochemistry, and immunofluorescence were used to determine the cellular origin and spatial distribution of TREM1. Using a co-culture model with TREM1 silenced, the potential impact of knocking down TAM-related TREM1 on suppressing malignant progression of glioma and its effect on macrophage polarization markers were evaluated through CCK-8, Transwell, wound healing assays, western blot, and flow cytometry. Results: TREM1 expression was upregulated in glioma and enriched in subtypes with higher malignant potential, indicating its role as a potential prognostic biomarker. TREM1 was closely associated with M2-type macrophages and promoted their polarization towards the M2 subtype. Knockdown of TREM1 in macrophages reduced the proliferation, invasion, and migration capabilities of glioma cells. Conclusion: TREM1 serves as a TAM-related oncogenic biomarker that facilitates malignant progression and immune suppression in glioma by promoting M2 macrophage polarization. Targeting TREM1 may offer a novel strategy to enhance the efficacy of immunotherapy for glioma.
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