ArticleNeuro-oncology2020
ICOSLG-mediated regulatory T-cell expansion and IL-10 production promote progression of glioblastoma.
Article in Neuro-oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 70 citations in OpenAlex.
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- AI-based pathomics model predicts regulatory T cell infiltration and radiotherapy response in IDH-wild-type glioblastoma.Frontiers in immunology · 2026Article
- ICOSL: more than a trigger of ICOS function.Cell communication and signaling : CCS · 2025Review
- Comprehensive analysis of immune escape-related prognostic signature in high-grade glioma.Discover oncology · 2025Article
- Phenotypic variations in glioma stem cells: regulatory mechanisms and implications for therapeutic strategies.Journal of translational medicine · 2025Review
- Comprehensive Characterization of the Immune Microenvironment Based on Nested Resampling Machine Learning Framework Identifies TRAF3 Interacting Protein 3 as a Promising Regulator to Improve the Resistance to Immunotherapy in Glioma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Immune factors and their role in tumor aggressiveness in glioblastoma: Atypical cadherin FAT1 as a promising target for combating immune evasion.Cellular & molecular biology letters · 2025Review
- Chemoradiation-Altered Micromilieu of Glioblastoma Cells Particularly Impacts M1-like Macrophage Activation.International journal of molecular sciences · 2025Article
- Application of bioinformatics analysis to construct the prognostic model and immune-related gene characteristics of low-grade glioma.Discover oncology · 2025Article
- FcRn-silencing of IL-12Fc prevents toxicity of local IL-12 therapy and prolongs survival in experimental glioblastoma.Nature communications · 2025Article
- Tumor-infiltrating and circulating B cells mediate local and systemic immunomodulatory mechanisms in Glioblastoma.Journal of neuro-oncology · 2025Review
- Identification of Recurrence-associated Gene Signatures and Machine Learning-based Prediction in IDH-Wildtype Histological Glioblastoma.Journal of molecular neuroscience : MN · 2025Article
- Single-cell analysis reveals transcriptomic features and therapeutic targets in primary pulmonary lymphoepithelioma-like carcinoma.Communications biology · 2025Article
- Immune checkpoints in immune response to glioma: two sides of the same coin.Frontiers in immunology · 2025Review
- The role of progranulin in macrophages of a glioblastoma model.Journal of neuro-oncology · 2024Article
- UCHL3 induces radiation resistance and acquisition of mesenchymal phenotypes by deubiquitinating POLD4 in glioma stem cells.Cellular and molecular life sciences : CMLS · 2024Article
- Understanding the immunosuppressive microenvironment of glioma: mechanistic insights and clinical perspectives.Journal of hematology & oncology · 2024Review
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15 authors at 3 institutions in 3 countries.
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Abstract
backgroundTargeting immune checkpoint proteins has recently gained substantial attention due to the dramatic success of this strategy in clinical trials for some cancers. Inducible T-cell co-stimulator ligand (ICOSLG) is a member of the B7 family of immune regulatory ligands, expression of which in cancer is implicated in disease progression due to regulation of antitumor adaptive immunity. Although aberrant ICOSLG expression has been reported in glioma cells, the underlying mechanisms that promote glioblastoma (GBM) progression remain elusive.
methodsHere, we investigated a causal role for ICOSLG in GBM progression by analyzing ICOSLG expression in both human glioma tissues and patient-derived GBM sphere cells (GSCs). We further examined its immune modulatory effects and the underlying molecular mechanisms.
resultsBioinformatics analysis and GBM tissue microarray showed that upregulation of ICOSLG expression was associated with poor prognosis in patients with GBM. ICOSLG expression was upregulated preferentially in mesenchymal GSCs but not in proneural GSCs in a tumor necrosis factor-α/nuclear factor-kappaB-dependent manner. Furthermore, ICOSLG expression by mesenchymal GSCs promoted expansion of T cells that produced interleukin-10. Knockdown of the gene encoding ICOSLG markedly reduced GBM tumor growth in immune competent mice, with a concomitant downregulation of interleukin-10 levels in the tumor microenvironment.
conclusionsInhibition of the ICOSLG-inducible co-stimulator axis in GBM may provide a promising immunotherapeutic approach for suppressing a subset of GBM with an elevated mesenchymal signature.
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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.