ArticleThe Journal of experimental medicine1992
Interleukin 4 protects chronic lymphocytic leukemic B cells from death by apoptosis and upregulates Bcl-2 expression.
Article in The Journal of experimental medicine, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 349 citations in OpenAlex.
- Dual action of pimozide through lysosome disruption and inhibition of STATs induces apoptosis in chronic lymphocytic leukemia (CLL).Blood advances · 2026Article
- Advancing CAR T-cell therapy for chronic lymphocytic leukemia: exploring resistance mechanisms and the innovative strategies to overcome them.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- The role of Th17 cells in chronic lymphocytic leukemia: friend or foe?Blood advances · 2023Review
- Role of MicroRNA-502-3p in Human Diseases.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Advancements on the Multifaceted Roles of Sphingolipids in Hematological Malignancies.International journal of molecular sciences · 2022Review
- In Vitro and In Vivo Models of CLL-T Cell Interactions: Implications for Drug Testing.Cancers · 2022Review
- Tumour Microenvironment Stress Promotes the Development of Drug Resistance.Antioxidants (Basel, Switzerland) · 2021Review
- Cascade of immune mechanism and consequences of inflammatory disorders.Phytomedicine : international journal of phytotherapy and phytopharmacology · 2021Review
- Can Immunocompetence Be Restored in Chronic Lymphocytic Leukemia?Hematology/oncology clinics of North America · 2021Review
- CD4+ T cells sustain aggressive chronic lymphocytic leukemia in Eμ-TCL1 mice through a CD40L-independent mechanism.Blood advances · 2021Article
- Review
- Interleukin-4 Receptor Inhibition Targeting Metastasis Independent of Macrophages.Molecular cancer therapeutics · 2021Article
- BTK Inhibitors in Chronic Lymphocytic Leukemia: Biological Activity and Immune Effects.Frontiers in immunology · 2021Review
- Mechanisms of resistance to CAR T cell therapies.Seminars in cancer biology · 2020Review
- Clinico-Biological Implications of Modified Levels of Cytokines in Chronic Lymphocytic Leukemia: A Possible Therapeutic Role.Cancers · 2020Review
- Harnessing the Effects of BTKi on T Cells for Effective Immunotherapy against CLL.International journal of molecular sciences · 2019Review
- Age-related changes in the BACH2 and PRDM1 genes in lymphocytes from healthy donors and chronic lymphocytic leukemia patients.BMC cancer · 2019Article
- IL-4-dependent Jagged1 expression/processing is associated with survival of chronic lymphocytic leukemia cells but not with Notch activation.Cell death & disease · 2018Article
- Duvelisib, an oral dual PI3K-δ, γ inhibitor, shows clinical activity in indolent non-Hodgkin lymphoma in a phase 1 study.American journal of hematology · 2018Article
- Intracellular IL-4 and IFN-γ expression in iNKT cells from patients with chronic lymphocytic leukemia.Oncology letters · 2018Article
19 more citing papers are in PubMed but not listed here.
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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 chronic lymphocytic leukemia (B-CLL) is characterized by the accumulation of slow-dividing and long-lived monoclonal B cells arrested at the intermediate stage of their differentiation. We previously showed that interleukin 4 (IL-4) not only inhibits but also prevents the proliferation of B-CLL cells. We report here that IL-4 protects the B-CLL cells from death by apoptosis (programmed cell death [PCD]). IL-4 inhibits spontaneous and hydrocortisone (HC)-induced PCD of highly purified B cells from 12 unselected CLL patients, as shown by sustained cell viability and lack of DNA fragmentation. IL-1, -2, -3, -5, -6, -7, tumor necrosis factor alpha, and transforming growth factor beta have no protective effect. The in vitro rescue from apoptosis by IL-4 is reflected by an increased expression of Bcl-2 protein, a proto-oncogene directly involved in the prolongation of cell survival in vivo and in vitro. Hence, IL-4-treated B-CLL cells express significantly more Bcl-2 than unstimulated, HC-treated, or fresh B-CLL cells. Furthermore, subcutaneous injection of IL-4 into one CLL patient enhances Bcl-2 protein expression in the leukemic B cells. These data may suggest that IL-4 prevents apoptosis of B-CLL cells using a Bcl-2-dependent pathway. Given our recent observations that fresh T cells from B-CLL patients express IL-4 mRNA, we propose that IL-4 has an essential role in the pathogenesis of CLL disease, by preventing both the death and the proliferation of the malignant B cells.
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