ArticleCell communication and signaling : CCS2014
TCR-triggered extracellular superoxide production is not required for T-cell activation.
Article in Cell communication and signaling : CCS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Oxidative stress in cancer: from tumor and microenvironment remodeling to therapeutic frontiers.Molecular cancer · 2025Review
- Radiotherapy-induced alterations in tumor microenvironment: metabolism and immunity.Frontiers in cell and developmental biology · 2025Review
- Redox Regulation of LAT Enhances T Cell-Mediated Inflammation.Antioxidants (Basel, Switzerland) · 2024Article
- Treatment with Exogenously Added Catalase Alters CD8 T Cell Memory Differentiation and Function.Advanced biology · 2023Article
- Reactive oxygen species formation and its effect on CD4Frontiers in immunology · 2023Review
- Metabolic ROS Signaling: To Immunity and Beyond.Biochemistry. Biokhimiia · 2020Review
- Calcium regulation of T cell metabolismCurrent opinion in physiology · 2020Article
- Exophilin-5 regulates allergic airway inflammation by controlling IL-33-mediated Th2 responses.The Journal of clinical investigation · 2020Article
- Mitochondrial superoxide disrupts the metabolic and epigenetic landscape of CD4Redox biology · 2019Article
- 1-Pyrroline-5-carboxylate released by prostate Cancer cell inhibit T cell proliferation and function by targeting SHP1/cytochrome c oxidoreductase/ROS Axis.Journal for immunotherapy of cancer · 2018Article
- Influence of Inflammation in the Process of T Lymphocyte Differentiation: Proliferative, Metabolic, and Oxidative Changes.Frontiers in immunology · 2018Review
- Preferential uptake of antioxidant carbon nanoparticles by T lymphocytes for immunomodulation.Scientific reports · 2016Article
- T cells and reactive oxygen species.Journal of biomedical science · 2015Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn the last decade, reactive oxygen species (ROS) production has been shown to occur upon T-cell receptor (TCR) stimulation and to affect TCR-mediated signalling. However, the exact reactive species that are produced, how ROS are generated and their requirement for T-cell activation, proliferation or cytokine production remain unclear, especially in the case of primary human T cells. Moreover, several groups have questioned that ROS are produced upon TCR stimulation.
resultsTo shed some light onto this issue, we specifically measured superoxide production upon TCR ligation in primary human and mouse T lymphocytes. We showed that superoxide is indeed produced and released into the extracellular space. Antioxidants, such as superoxide dismutase and ascorbate, abolished superoxide production, but surprisingly did not affect activation, proliferation and cytokine secretion in TCR-stimulated primary human T cells. It has been suggested that T cells produce ROS via the NADPH oxidase 2 (NOX2). Therefore, we investigated whether T-cell activation is affected in NOX2-deficient mice (gp91phox-/-). We found that T cells from these mice completely lack inducible superoxide production but display normal upregulation of activation markers and proliferation.
conclusionsCollectively, our data indicate that primary T cells produce extracellular superoxide upon TCR triggering, potentially via NOX2 at the plasma membrane. However, superoxide is not required for T-cell activation, proliferation and cytokine production.
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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 OpenQuestion graph.