MINI REVIEW article
Front. Immunol.
Sec. Molecular Innate Immunity
From Neuroinflammation to Gliomagenesis: Immune Drivers of Malignant Transformation in the CNS
Provisionally accepted
- 1Suzhou Ninth People's Hospital, Suzhou, China
- 2The Second Clinical Medical College, Nanjing Medical University, Nanjing, China
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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.
Keywords: gliomagenesis, Neuroinflammation, Microglia, Immunosuppression, STAT3 signaling, Glioma-initiating cells
Received: 08 Aug 2025; Accepted: 14 Nov 2025.
Copyright: © 2025 Bao, Su, Chen, Guo, Du and Jia. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Huaping Du, duhuaping226@126.com
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