ArticleCell death & disease2016
Glutathione peroxidase 1 deficiency attenuates concanavalin A-induced hepatic injury by modulation of T-cell activation.
Article in Cell death & disease, 2016. 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, 35 citations in OpenAlex.
- ROS-Responsive Nanoplatforms for Targeted Tumor Immunomodulation: A Paradigm Shift in Precision Cancer Immunotherapy.Pharmaceutics · 2025Review
- Tumor Vasculature as an Emerging Pharmacological Target to Promote Anti-Tumor Immunity.International journal of molecular sciences · 2023Review
- Redox regulation of the immune response.Cellular & molecular immunology · 2022Review
- Mitigation of DSS-Induced Colitis Potentially via Th1/Th2 Cytokine and Immunological Function Balance Induced by Phenolic-Enriched Buckwheat (Foods (Basel, Switzerland) · 2022Article
- Selenoproteins as regulators of T cell proliferation, differentiation, and metabolism.Seminars in cell & developmental biology · 2021Article
- Arginine-dependent immune responses.Cellular and molecular life sciences : CMLS · 2021Review
- Redox regulation of immunometabolism.Nature reviews. Immunology · 2021Review
- Effects of Injectable Trace Minerals (ITMs) on Th1/Th2 Cytokine Balance of Newborn Calves with Tropical Theileriosis.Biological trace element research · 2021Article
- Review
- High-throughput single-cell live imaging of photobiomodulation with multispectral near-infrared lasers in cultured T cells.Journal of biomedical optics · 2020Article
- Redox Control of the Immune Response in the Hepatic Progenitor Cell Niche.Frontiers in cell and developmental biology · 2020Article
- Protective Function of Novel Fungal Immunomodulatory Proteins Fip-lti1 and Fip-lti2 fromOxidative medicine and cellular longevity · 2019Article
- Mitochondrial stress management: a dynamic journey.Cell stress · 2018Review
- The emerging role of immune dysfunction in mitochondrial diseases as a paradigm for understanding immunometabolism.Metabolism: clinical and experimental · 2018Review
- The Role of Reactive Oxygen Species in Regulating T Cell-mediated Immunity and Disease.Immune network · 2018Review
- MiR-21 is required for anti-tumor immune response in mice: an implication for its bi-directional roles.Oncogene · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Concanavalin A (Con A)-induced hepatitis model is well-established experimental T cell-mediated liver disease. Reactive oxygen species (ROS) is associated with T-cell activation and proliferation, but continued ROS exposure induces T-cell hyporesponsiveness. Because glutathione peroxidase 1 (Gpx1) is an antioxidant enzyme and is involved in T-cell development, we investigated the role of Gpx1 during Con A-induced liver injury in Gpx1 knockout (KO) mice. Male wild-type (WT) mice and Gpx1 KO mice were intravenously injected with Con A (10 mg/kg), and then killed after 8 h after Con A injection. Serum levels of aspartate transaminase and alanine transaminase were measured to assess hepatic injury. To identify that Gpx1 affects T cell-mediated inflammation, we pretreated Gpx1 inhibitor to Human Jurkat T cells then treated Con A. Con A-induced massive liver damage in WT mice but its damage was attenuated in Gpx1 KO mice. Con A-induced Th1 cytokines such as tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ) and interleukin (IL)-2 were also decreased in the liver and spleen of Gpx1 KO mice compared with WT mice. In Jurkat T cells, Con A-induced mRNA levels of IL-2, IFN-γ and TNF-α were downregulated by pretreatment of Gpx inhibitor, mercaptosuccinic acid. We also observed that Gpx1 KO mice showed increasing oxidative stress in the liver and spleen compared with WT mice. These results suggest that Gpx1 deficiency attenuates Con A-induced liver injury by induction of T-cell hyporesponsiveness through chronic ROS exposure.
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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.