ArticleOncotarget2015
Natural killer cells facilitate PRAME-specific T-cell reactivity against neuroblastoma.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Circumventing IFN-γ induced resistance in ovarian cancer with a double-hit: NKG2A knockout of PRAME-TCR expressing NK cells.Journal of ovarian research · 2026Article
- Shared PRAME epitopes are T-cell targets in NUT carcinoma.Journal for immunotherapy of cancer · 2026Article
- CAR T cell-induced interferon gamma enhances MHC class I expression and sensitizes neuroblastoma to TCR-engineered T cell therapy.Frontiers in immunology · 2026Article
- T cells in the microenvironment of solid pediatric tumors: the case of neuroblastoma.Frontiers in immunology · 2025Review
- Review
- Thymic NK-Cells and Their Potential in Cancer Immunotherapy.ImmunoTargets and therapy · 2024Review
- Strategies to overcome low MHC-I expression in paediatric and adult tumours.Immunotherapy advances · 2024Review
- Review
- Biological Insight and Recent Advancement in the Treatment of Neuroblastoma.International journal of molecular sciences · 2023Review
- A combined immunopeptidomics, proteomics, and cell surface proteomics approach to identify immunotherapy targets for diffuse intrinsic pontine glioma.Frontiers in oncology · 2023Article
- Mechanisms of immune modulation in the tumor microenvironment and implications for targeted therapy.Frontiers in oncology · 2023Review
- Epigenetic modulation of neuroblastoma enhances T cell and NK cell immunogenicity by inducing a tumor-cell lineage switch.Journal for immunotherapy of cancer · 2022Article
- Mesenchymal and adrenergic cell lineage states in neuroblastoma possess distinct immunogenic phenotypes.Nature cancer · 2022Article
- Stress increases MHC-I expression in dopaminergic neurons and induces autoimmune activation in Parkinson's disease.Neural regeneration research · 2021Article
- αβ-T Cells Engineered to Express γδ-T Cell Receptors Can Kill Neuroblastoma Organoids Independent of MHC-I Expression.Journal of personalized medicine · 2021Article
- Can Immune Suppression and Epigenome Regulation in Placenta Offer Novel Insights into Cancer Immune Evasion and Immunotherapy Resistance?Epigenomes · 2021Review
- Advances in immunotherapeutic targets for childhood cancers: A focus on glypican-2 and B7-H3.Pharmacology & therapeutics · 2021Review
- Novel Treatments and Technologies Applied to the Cure of Neuroblastoma.Children (Basel, Switzerland) · 2021Review
- Review
- Cancer Testis Antigens and Immunotherapy: Expression of PRAME Is Associated with Prognosis in Soft Tissue Sarcoma.Cancers · 2020Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroblastoma is the most common solid tumor in children with an estimated 5-year progression free survival of 20-40% in stage 4 disease. Neuroblastoma actively avoids recognition by natural killer (NK) cells and cytotoxic T lymphocytes (CTLs). Although immunotherapy has gained traction for neuroblastoma treatment, these immune escape mechanisms restrain clinical results. Therefore, we aimed to improve neuroblastoma immunogenicity to further the development of antigen-specific immunotherapy against neuroblastoma. We found that neuroblastoma cells significantly increase surface expression of MHC I upon exposure to active NK cells which thereby readily sensitize neuroblastoma cells for recognition by CTLs. We show that oncoprotein PRAME serves as an immunodominant antigen for neuroblastoma as NK-modulated neuroblastoma cells are recognized by PRAMESLLQHLIGL/A2-specific CTL clones. Furthermore, NK cells induce MHC I upregulation in neuroblastoma through contact-dependent secretion of IFNγ. Our results demonstrate remarkable plasticity in the peptide/MHC I surface expression of neuroblastoma cells, which is reversed when neuroblastoma cells experience innate immune attack by sensitized NK cells. These findings support the exploration of NK cells as adjuvant therapy to enforce neuroblastoma-specific CTL responses.
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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.