ArticleCancer immunology, immunotherapy : CII2025
GD2-CAR NK-92 cell activity against neuroblastoma cells is insusceptible to TIGIT knockout.
Article in Cancer immunology, immunotherapy : CII, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Bioengineered cell therapies for pediatric solid tumors: unmet needs and a measurement-integrated approach.Progress in biomedical engineering (Bristol, England) · 2026Review
- Targeting GD2 with CAR-T Cell Therapy in Neuroblastoma: Updates, Challenges, and Future Perspectives.Current oncology reports · 2026Review
- Management of persistent soft tissue residuals exhibiting an imaging paradox (^123I-MIBG-negative/^68Ga-DOTA-NOC-positive) in high-risk neuroblastoma following immunotherapy: a case report.Frontiers in immunology · 2026Article
- Overcoming barriers in CAR-NK immunotherapy: CRISPR-Driven advances in checkpoint editing and allogeneic design.Functional & integrative genomics · 2025Review
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Authors and funding
7 authors.
Funding
Abstract
Immunotherapy by inhibition of immune checkpoint (IC) molecules has emerged as an important cancer therapy. Among these lC, the poliovirus receptor/poliovirus receptor-like 2 protein (PVR/PVRL2)-TIGIT axis was discovered as potential target for various cancers. For neuroblastoma (NB), the most common extracranial solid cancer in children, no effective IC therapy has been established yet. To investigate the PVR/PVRL2-TIGIT IC axis as a new target for the treatment of NB, we analysed whether PVR and PVRL2 influence the survival of patients and verified the expression of the receptors on NB cell lines. To disrupt the checkpoint axis, we performed single and double knockouts of these receptors on NB cell lines and subsequently removed TIGIT, an inhibitory receptor on immune effector cells, from NK-92 cells. Finally, we combined checkpoint inhibition with GD2-CAR NK-92 cells and investigated changes in cytotoxicity. Using RNA-Seq data we showed that the expression of PVR and PVRL2 on NB cells correlates to a lower event-free survival of patients. CRISPR/Cas9 knockouts of PVR and PVRL2 showed no improved cytotoxic activity of NK-92 cells. We observed enhanced lysis of NB cells using TIGIT-deficient NK-92 cells. However, the cytotoxicity of GD2-CAR NK-92 was not significantly enhanced. In summary, we have shown that in addition to the interaction of PVR/PVRL2 and TIGIT on engineered immune effector cells against NB, pleiotropic ligands appear to be relevant. Deletion of TIGIT from immune effector cells is a promising approach to protect these cells from tumour-associated inhibitory signals but cannot enhance the effect of GD2-CAR-NK-92 cells.
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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.