ArticleJournal for immunotherapy of cancer2022
LRIG2 promotes glioblastoma progression by modulating innate antitumor immunity through macrophage infiltration and polarization.
Article in Journal for immunotherapy of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- LRIG2 suppresses NK cell-induced GSDME-mediated pyroptosis via the LAMP1-STAT3 pathway in glioma.Journal for immunotherapy of cancer · 2026Article
- Targeting regulatory T cells in glioblastoma: from mechanistic insights to novel immunotherapeutic strategies.Frontiers in immunology · 2026Review
- Decoding the immune microenvironment: precision immunotherapy for medulloblastoma subtypes.Frontiers in immunology · 2026Review
- Deciphering the role of CD47 in cancer immunotherapy.Journal of advanced research · 2024Review
- Phagocytosis Checkpoints in Glioblastoma: CD47 and Beyond.Current issues in molecular biology · 2024Review
- The Tumor Immune Microenvironment in Primary CNS Neoplasms: A Review of Current Knowledge and Therapeutic Approaches.International journal of molecular sciences · 2023Review
- Glioma-derived LRIG3 interacts with NETO2 in tumor-associated macrophages to modulate microenvironment and suppress tumor growth.Cell death & disease · 2023Article
- Glioma-associated microglia/macrophages (GAMs) in glioblastoma: Immune function in the tumor microenvironment and implications for immunotherapy.Frontiers in immunology · 2023Review
- Microglia and Brain Macrophages as Drivers of Glioma Progression.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
21 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastoma (GBM) is the most common malignant brain tumor with poor clinical outcomes. Immunotherapy has recently been an attractive and promising treatment of extracranial malignancies, however, most of clinical trials for GBM immunotherapy failed due to predominant accumulation of tumor-associated microglia/macrophages (TAMs).
resultsHigh level of LRIG2/soluble LRIG2 (sLRIG2) expression activates immune-related signaling pathways, which are associated with poor prognosis in GBM patients. LRIG2/sLRIGs promotes CD47 expression and facilitates TAM recruitment. Blockade of CD47-SIRPα interactions and inhibition of sLRIG2 secretion synergistically suppress GBM progression in an orthotropic murine GBM model.
conclusionsGBM cells with high level LRIG2 escape the phagocytosis by TAM via the CD47-SIRPα axis, highlighting a necessity for an early stage of clinical trial targeting LRIG2 and CD47-SIRPα as a novel treatment for patients with GBM.
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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.