ArticleCell death and differentiation2014
IL-15 maintains T-cell survival via S-nitrosylation-mediated inhibition of caspase-3.
Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- A human tumor-immune organoid model of glioblastoma.Cell reports · 2026Article
- Modeling immunotherapies in live 3D human cancer tissue bioreactors.Theranostics · 2026Article
- A Human Tumor-Immune Organoid Model of Glioblastoma.bioRxiv : the preprint server for biology · 2025Article
- Molecular and temporal control of restimulation-induced cell death (RICD) in T lymphocytes.Frontiers in cell death · 2023Article
- Mitochondrial reactive oxygen is critical for IL-12/IL-18-induced IFN-γ production by CD4Cell death & disease · 2022Article
- Endogenous Hydrogen Sulfide Persulfidates Caspase-3 at Cysteine 163 to Inhibit Doxorubicin-Induced Cardiomyocyte Apoptosis.Oxidative medicine and cellular longevity · 2022Article
- Cancer Metabolism: The Role of Immune Cells Epigenetic Alteration in Tumorigenesis, Progression, and Metastasis of Glioma.Frontiers in immunology · 2022Review
- IL15 Enhances CAR-T Cell Antitumor Activity by Reducing mTORC1 Activity and Preserving Their Stem Cell Memory Phenotype.Cancer immunology research · 2019Article
- Article
- Glycolysis Induces MCJ Expression That Links T Cell Proliferation With Caspase-3 Activity and Death.Frontiers in cell and developmental biology · 2019Article
- Review
- Glycolysis promotes caspase-3 activation in lipid rafts in T cells.Cell death & disease · 2018Article
- Characterization of NO-Induced Nitrosative Status in Human Placenta from Pregnant Women with Gestational Diabetes Mellitus.Oxidative medicine and cellular longevity · 2017Article
- Article
- HIV-1 pathogenicity and virion production are dependent on the metabolic phenotype of activated CD4+ T cells.Retrovirology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Caspase activity is critical for both T-cell survival and death. However, little is known regarding what determines caspase activity in cycling T cells. Interleukin (IL)-2 and IL-15 confer very different susceptibilities to T-cell death. We therefore considered that IL-2 and IL-15 differentially regulate caspase activity to influence T-cell survival. We observed that IL-2-cultured primary murine effector T cells manifested elevated levels of caspase-3 activity compared with IL-15-cultured T cells. T cell receptor (TCR) restimulation further increased caspase activity and induced considerable cell death in IL-2-cultured T cells, but provoked only a minimal increase of caspase activity and cell death in IL-15-cultured T cells. IL-2 sensitization to cell death was caspase-3 mediated. Interestingly, increased active caspase-3 levels with IL-2 were independent of active initiator caspase-8 and caspase-9 that were similar with IL-2 and IL-15. Rather, caspase-3 activity was inhibited by posttranslational S-nitrosylation in IL-15-cultured T cells, but not in the presence of IL-2. This paralleled increased reactive nitrogen and oxygen species with IL-15 and reduced glycolysis. Taken together, these data suggest that the metabolic state conferred by IL-15 inhibits T-cell apoptosis in part by maintaining low levels of active caspase-3 via S-nitrosylation.
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