ArticleArthritis & rheumatology (Hoboken, N.J.)2022
Role of Glutaminase 2 in Promoting CD4+ T Cell Production of Interleukin-2 by Supporting Antioxidant Defense in Systemic Lupus Erythematosus.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2022. 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, 17 citations in OpenAlex.
- Ferroptosis in T cells: mechanisms, biology and translational opportunities.Nature reviews. Immunology · 2026Review
- Metabolomics Reveals Potential Biomarkers for Early Detection of irAEs in ICI-Treated Patients.Drug design, development and therapy · 2026Article
- Cuproptosis: A Potential Target for the Treatment of Systemic Lupus Erythematosus.Journal of inflammation research · 2026Review
- Reprogramming CAR T cells across genetic, epigenetic, metabolic and microenvironmental axes to improve efficacy and safety in cancer and autoimmune disease.Frontiers in immunology · 2026Review
- Inhibition of bruton's tyrosine kinase directly alleviates pathogenic CD4+ T cell response via PPAR-γ signaling in autoimmune uveitis.Journal of neuroinflammation · 2025Article
- Metabolic pathways within cTfh subsets and glucose-dependent activation of cTfh17 in SLE and healthy individuals.JCI insight · 2025Article
- Ten-Eleven Translocation Family Proteins: Structure, Biological Functions, Diseases, and Targeted Therapy.MedComm · 2025Review
- Screening and validating genes associated with cuproptosis in systemic lupus erythematosus by expression profiling combined with machine learning.Biomolecules & biomedicine · 2025Article
- Ferroptosis of T cell in inflammation and tumour immunity.Clinical and translational medicine · 2025Review
- Immunocyte lipid metabolic reprogramming: a novel pathway for targeted intervention in autoimmune diseases.Frontiers in immunology · 2025Review
- α-Ketoglutarate-Dependent KDM6 Histone Demethylases and Interferon-Stimulated Gene Expression in Lupus.Arthritis & rheumatology (Hoboken, N.J.) · 2024Article
- Glutaminolysis of CD4Journal of inflammation research · 2024Review
- Functional Genome Analysis for Immune Cells Provides Clues for Stratification of Systemic Lupus Erythematosus.Biomolecules · 2023Review
- Regulatory T cell homeostasis: Requisite signals and implications for clinical development of biologics.Clinical immunology (Orlando, Fla.) · 2023Review
- Glutaminolysis and CD4Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
objectiveGlutaminase (GLS) isoenzymes GLS1 and GLS2 catalyze the first step of glutaminolysis. GLS1 is requisite for Th17 cell differentiation, and its inhibition suppresses autoimmune disease in animals, but the function of GLS2 is not known. The aim of this study was to investigate the role of GLS2 in CD4+ T cell function and systemic lupus erythematosus (SLE) pathogenesis.
methodsWe measured reactive oxygen species (ROS) levels, lipid peroxidation, and mitochondrial mass and polarization by flow cytometry, interleukin-2 (IL-2) production by a dual luciferase assay, and CpG DNA methylation of Il2 by a real-time polymerase chain reaction system. The impact of the overexpression of wild-type GLS1, wild-type GLS2, or mutated GLS2 at the PDZ domain-binding motif in CD4+ T cells was examined. Furthermore, GLS2 expression in CD4+ T cells from lupus-prone mice and patients with SLE was analyzed by Western blotting.
resultsGLS2, but not GLS1, reduced ROS levels and lipid peroxidation and restored mitochondrial function in T cells. GLS2 promoted IL-2 production through the demethylation of the Il2 promoter. Mutation of the PDZ domain-binding motif abated the ability of GLS2 to regulate IL-2 and ROS levels. In lupus-prone mice and patients with SLE, the expression of GLS2 was decreased in CD4+ T cells. Finally, GLS2 overexpression corrected ROS levels and restored IL-2 production by CD4+ T cells from lupus-prone mice and SLE patients.
conclusionOur findings suggest that GLS2 has a crucial role in IL-2 production by CD4+ T cells by supporting antioxidant defense, and they offer a new approach to correcting IL-2 production by T cells in SLE.
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