ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Single-Cell Transcriptome Atlas Reveals the Underlying Mechanism of Kynurenic Acid in the Regulation of Tumor Immune Microenvironment in Glioblastoma.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Single-Cell Transcriptome Atlas Reveals the Underlying Mechanism of Kynurenic Acid in the Regulation of Tumor Immune Microenvironment in Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
Tryptophan metabolism plays a critical role in glioblastoma (GBM), however, the regulatory functions of kynurenic acid (KYNA) in this context remain poorly understood. Using an in-house clinical cohort, targeted metabolomic analysis revealed significantly downregulated KYNA levels in GBM tissues compared to non-tumor brain tissues. Further investigation demonstrated that KYNA administration markedly reduced tumor burden in an orthotopic GBM mouse model. Through integrated cytometry by time-of-fight (CyTOF), single-cell RNA sequencing (scRNA-seq), proteome, and flow cytometry analyses, this study delineated the alterative tumor immune landscape following KYNA treatment. Specifically, KYNA remodeled the immunosuppressive myeloid compartment within the GBM microenvironment. Additionally, KYNA reversed T cell exhaustion signatures, enhanced cytotoxic function, thereby augmented anti-tumor T cell responses. Notably, the anti-tumor effects of KYNA are abrogated in T cell-deficient mouse models (nude and Rag2-/-), confirming its dependence on adaptive immunity. In summary, this study highlights the therapeutic potential of KYNA in GBM and provides a comprehensive, multi-omics-based understanding of its immunomodulatory mechanisms.
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Registered trials
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