ArticleMolecular therapy. Oncology2024
Deletion of CD38 enhances CD19 chimeric antigen receptor T cell function.
Article in Molecular therapy. Oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The trial behind it
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Who cites it
9 citing papers in PubMed.
- Augmenting CAR T cell functionality and metabolism through CD39 downtuning.Molecular therapy. Oncology · 2026Article
- Allo-defensive, multiplex base-edited, anti-CD38 CAR T cells for 'off-the-shelf' immunotherapy.Haematologica · 2026Article
- CAR-T cells with the CD38Cell reports. Medicine · 2026Article
- Overcoming resistance to immunotherapy by targeting CD38 in human tumor explants.Cell reports. Medicine · 2025Article
- Characterization of the aryl hydrocarbon receptor as a potential candidate to improve cancer T cell therapies.Cancer immunology, immunotherapy : CII · 2025Article
- LLT1 overexpression renders allogeneic-NK resistance and facilitates the generation of enhanced universal CAR-T cells.Journal of experimental & clinical cancer research : CR · 2025Article
- CD38 promotes LPS-induced innate-like activation and proliferation of CD8Frontiers in aging · 2025Article
- CD38 deletion to preserve CAR T cell metabolism and promote functional persistence.Molecular therapy. Oncology · 2024Article
- Novel gene manipulation approaches to unlock the existing bottlenecks of CAR-NK cell therapy.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell surface molecules transiently upregulated on activated T cells can play a counter-regulatory role by inhibiting T cell function. Deletion or blockade of such immune checkpoint receptors has been investigated to improve the function of engineered immune effector cells. CD38 is upregulated on activated T cells, and although there have been studies showing that CD38 can play an inhibitory role in T cells, how it does so has not fully been elucidated. In comparison with molecules such as PD1, CTLA4, LAG3, and TIM3, we found that CD38 displays more sustained and intense expression following acute activation. After deleting CD38 from human chimeric antigen receptor (CAR) T cells, we showed relative resistance to exhaustion
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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.