ReviewFrontiers in immunology2025
From neuroinflammation to gliomagenesis: immune drivers of malignant transformation in the CNS.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Natural Product Rengyolone Attenuates LPS-Induced Microglia Inflammation via Suppression of the TLR4/NF-κB Pathway.Chemistry & biodiversity · 2026Article
- Nervous and immune system crosstalk shapes cancer progression and treatment response.Discover oncology · 2026Review
- Mechanisms and therapeutic strategies of bidirectional crosstalk between hepatic stellate cell-derived cancer-associated fibroblasts and T cells in immune evasion and therapeutic resistance of hepatocellular carcinoma.Frontiers in immunology · 2026Review
- Chimeric antigen receptor macrophages therapy for glioblastoma: challenges and opportunities from preclinical evidence to clinical translation.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic neuroinflammation is increasingly recognized not merely as a consequence of CNS pathology but as a driver of glioma initiation. Sustained immune activation, induced by trauma, infection, or neurodegeneration, reshapes the brain's immune milieu in ways that favor malignant transformation. Persistent inflammation activates glial cells, triggers cytokine release, and disrupts the blood-brain barrier, permitting immune infiltration and dysfunction. These changes promote the accumulation and reprogramming of immunosuppressive populations, including regulatory T cells and myeloid-derived suppressor cells, while resident microglia and astrocytes adopt tumor-supportive phenotypes. We highlight signaling axes such as IL-6/STAT3, NF-κB, and TGF-β that connect immune dysregulation to epigenetic instability and the emergence of glioma-initiating cells. By tracing the progression from inflammation to tumorigenesis, we identify opportunities for early immune-based intervention, particularly in individuals with chronic neuroinflammatory conditions.
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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.