ArticleFrontiers in immunology2023
Ibrutinib directly reduces CD8+T cell exhaustion independent of BTK.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 9 citations in OpenAlex.
- Decoding IGLL5 Mutation-Mediated BCR Signaling: A Novel Mechanism of CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Upregulation of TCF1 and BCL11B in CD8+ effector T cells predicts favorable response to ibrutinib in patients with chronic lymphocytic leukemia.Communications biology · 2026Article
- Mechanisms of resistance to bruton's tyrosine kinase inhibitors: synergistic effects of tumor microenvironment regulation and signaling pathways.Annals of hematology · 2026Review
- Expanded CD16Scientific reports · 2025Article
- Inhibition of head and neck squamous cell carcinoma by Bruton's tyrosine kinase inhibitor ibrutinib is associated with reduction of immunosuppressive T cells.Cancer immunology, immunotherapy : CII · 2025Article
- Leveraging the Immunomodulatory Potential of Ibrutinib for Improved Outcomes of T Cell-Mediated Therapies of B Cell Malignancies: A Narrative Review.Targeted oncology · 2025Review
- Ibrutinib disrupts blood-tumor barrier integrity and prolongs survival in rodent glioma model.Acta neuropathologica communications · 2024Article
- Small molecule inhibitors as adjuvants in cancer immunotherapy: enhancing efficacy and overcoming resistance.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Cytotoxic CD8+ T cell (CTL) exhaustion is a dysfunctional state of T cells triggered by persistent antigen stimulation, with the characteristics of increased inhibitory receptors, impaired cytokine production and a distinct transcriptional profile. Evidence from immune checkpoint blockade therapy supports that reversing T cell exhaustion is a promising strategy in cancer treatment. Ibrutinib, is a potent inhibitor of BTK, which has been approved for the treatment of chronic lymphocytic leukemia. Previous studies have reported improved function of T cells in ibrutinib long-term treated patients but the mechanism remains unclear. We investigated whether ibrutinib directly acts on CD8+ T cells and reinvigorates exhausted CTLs. Methods: We used an established Results: We found that ibrutinib reduced exhaustion-related features of CTLs in an Discussion: Our study demonstrates that ibrutinib directly ameliorates CTL exhaustion, and provides evidence for its synergistic use with cancer immunotherapy.
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What OpenQuestion holds
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.