ArticleiScience2024
Type I interferon signaling regulates myeloid and T cell crosstalk in the glioblastoma tumor microenvironment.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Baseline IL-6, IL-8, IFN-ω, and perforin as prognostic biomarkers in immune checkpoint inhibitor-treated metastatic non-small cell lung cancer.Translational lung cancer research · 2026Article
- Persistent IFN-I signaling associated with the HIV-1 reservoir fuels immune exhaustion and reveals therapeutic targets.Frontiers in immunology · 2026Review
- Comprehensive pan-cancer analysis of p62 reveals its contribution to shaping tumor microenvironment and anti-tumor immunity.Discover oncology · 2025Article
- Targeting DNA Damage Response and Immune Crosstalk in Cancer: Mechanistic Insights and Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Claudin-4 as a dual regulator of genome stability and immune evasion in high grade serous ovarian cancer.Scientific reports · 2025Article
- PINK1 deficiency rewires early immune responses in a mouse model of Parkinson's disease triggered by intestinal infection.NPJ Parkinson's disease · 2025Article
- METTL3 depletion blocks vesicular stomatitis virus replication in pancreatic cancer cells through the establishment of an intrinsic antiviral state.Journal of virology · 2025Article
- The role of type I interferon signaling in myeloid anti-tumor immunity.Frontiers in immunology · 2025Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Downstream interferon signaling through the type I interferon (IFN) receptor, IFNAR, is crucial for the proper production of type I IFNs in mounting anti-tumor immune responses. Our study investigates the role of type I IFN signaling in the glioblastoma (GBM) tumor microenvironment by leveraging single-cell RNA sequencing to analyze tumor-infiltrating lymphocytes. We investigate how type I IFN signaling within the myeloid compartment contributes to the crosstalk with T cells in the tumor microenvironment. Through the use of the Gl261 murine GBM model, we find that the lack of proper type I IFN response results in enhanced PD-L1 interactions among myeloid cells, thereby affecting T cell functionality. Additionally, we also characterize how anti-PD1 treatment induces transcriptional changes in tumor-associated monocytes and macrophages by analyzing intercellular communication networks and propose how immune checkpoint blockade therapy could possibly relieve some of the immunosuppression derived from the lack of proper type I IFN production.
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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.