ArticleFrontiers in immunology2021
The PI3K∂-Selective Inhibitor Idelalisib Induces T- and NK-Cell Dysfunction Independently of B-Cell Malignancy-Associated Immunosuppression.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
- Utility of mouse precision cut lung slices as an in vitro model for interrogating the lung immune response against bacterial pathogens in the context of immunomodulatory therapeutics.Respiratory research · 2026Article
- The PI3Kδ inhibitor roginolisib (IOA-244) preserves T-cell function and activity.Molecular oncology · 2026Article
- Leveraging Macrophage Metabolic Reprogramming for Enhanced Anti-Tumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Insights into PI3K/AKT signaling in B cell development and chronic lymphocytic leukemia.FEBS letters · 2025Review
- Review
- Best Supportive Care for Patients with Chronic Lymphocytic Leukemia: Relevance of Cancer Screening and Immunizations.Cancers · 2025Review
- Overexpressing natural killer group 2 member A drives natural killer cell exhaustion in relapsed acute myeloid leukemia.Signal transduction and targeted therapy · 2025Article
- NK cell-related genes-driven novel molecular subtyping and prognostic signatures for Wilms tumor: uncovering the therapeutic potential of TGX-221 and biomarker role of HS2ST1.Frontiers in oncology · 2025Article
- Article
- Managing novel therapies and concomitant medications in chronic lymphocytic leukemia: key challenges.Frontiers in pharmacology · 2024Review
- Simultaneous Inhibition of PI3Kgamma and PI3Kdelta Deteriorates T-cell Function With Implications for Chronic Lymphocytic Leukemia.HemaSphere · 2023Article
- Development and safety of PI3K inhibitors in cancer.Archives of toxicology · 2023Review
- Natural Killer Cells in Chronic Lymphocytic Leukemia: Functional Impairment and Therapeutic Potential.Cancers · 2022Review
- Immune Modulatory Effects of Molecularly Targeted Therapy and Its Repurposed Usage in Cancer Immunotherapy.Pharmaceutics · 2022Review
- Pathological Mechanism and Targeted Drugs of COPD.International journal of chronic obstructive pulmonary disease · 2022Review
- Regulatory T cells (Tregs) in lymphoid malignancies and the impact of novel therapies.Frontiers in immunology · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B-cell receptors, multiple receptor tyrosine kinases, and downstream effectors are constitutively active in chronic lymphocytic leukemia (CLL) B cells. Activation of these pathways results in resistance to apoptosis and enhanced survival of the leukemic cells. Idelalisib is a highly selective inhibitor of the PI3K p110∂ isoform and is approved for the treatment of CLL in patients with relapsed/refractory disease or in those harboring 17p deletions or tp53 mutations. Despite the initial excitement centered around high response rates in clinical trials of idelalisib, its therapeutic success has been hindered by the incidence of severe opportunistic infections. To examine the potential contribution of idelalisib to the increased risk of infection, we investigated the effects of idelalisib on the immune cell compartments of healthy donors (HDs) and CLL patients. PI3K∂ blockade by idelalisib reduced the expression levels of inhibitory checkpoint molecules in T cells isolated from both HDs and CLL patients. In addition, the presence of idelalisib in cultures significantly decreased T-cell-mediated cytotoxicity and granzyme B secretion, as well as cytokine secretion levels in both cohorts. Furthermore, idelalisib reduced the proliferation and cytotoxicity of HD NK cells. Collectively, our data demonstrate that both human T and NK cells are highly sensitive to PI3K∂ inhibition. Idelalisib interfered with the functions of T and NK cell cells from both HDs and CLL patients. Therefore, idelalisib might contribute to an increased risk of infections regardless of the underlying B-cell malignancy.
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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 Socratic graph.