ArticleEuropean journal of immunology2012
Decreased STAT5 phosphorylation and GATA-3 expression in NOX2-deficient T cells: role in T helper development.
Article in European journal of immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Boosting T cell antioxidant capacity: A strategic approach to overcome immunosuppression in solid tumors.Redox biology · 2026Review
- Th17 cells require the DNA repair sensor xeroderma pigmentosum complementation Group C to control oxidative DNA damage in a murine model.Nature communications · 2026Article
- Intracellular Oxidant Levels Are Crucial for Cell Survival and JAK/STAT Signaling in Classical Hodgkin's Lymphoma.Antioxidants (Basel, Switzerland) · 2026Article
- Article
- Panoramic description of ROS-based nanotechnology for osteomyelitis therapy: Challenges, opportunities, and prospects.Theranostics · 2026Review
- The type 1 and type 3 immune responses underlying the tissue inflammation associated with NOX2 deficiency.Frontiers in immunology · 2026Review
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Intact NOX2 in T Cells Mediates Pregnancy-Induced Renal Damage in Dahl SS Rats.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Article
- Dieckol Reduces Muscle Atrophy by Modulating Angiotensin Type II Type 1 Receptor and NADPH Oxidase in Spontaneously Hypertensive Rats.Antioxidants (Basel, Switzerland) · 2021Article
- Selenoproteins as regulators of T cell proliferation, differentiation, and metabolism.Seminars in cell & developmental biology · 2021Article
- The Redox-Metabolic Couple of T Lymphocytes: Potential Consequences for Hypertension.Antioxidants & redox signaling · 2021Review
- Reactive Oxygen Species in Autoimmune Cells: Function, Differentiation, and Metabolism.Frontiers in immunology · 2021Review
- Beyond the Extra Respiration of Phagocytosis: NADPH Oxidase 2 in Adaptive Immunity and Inflammation.Frontiers in immunology · 2021Review
- Metabolic Reprogramming and Reactive Oxygen Species in T Cell Immunity.Frontiers in immunology · 2021Review
- Metabolic Reprogramming in Modulating T Cell Reactive Oxygen Species Generation and Antioxidant Capacity.Frontiers in immunology · 2018Review
- Influence of Inflammation in the Process of T Lymphocyte Differentiation: Proliferative, Metabolic, and Oxidative Changes.Frontiers in immunology · 2018Review
- Major CD4 T-Cell Depletion and Immune Senescence in a Patient with Chronic Granulomatous Disease.Frontiers in immunology · 2017Article
- Clinical significance of T cell metabolic reprogramming in cancer.Clinical and translational medicine · 2016Review
- Computational properties of mitochondria in T cell activation and fate.Open biology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Absence of phagocyte NADPH oxidase (NOX2) activity causes chronic granulomatous disease (CGD), a primary immunodeficiency characterized by recurrent bacterial infections. In contrast to this innate immune deficit, CGD patients and animal models display a predisposition toward autoimmune disease and enhanced response to Helicobacter pylori and influenza virus infection. These data imply an altered, perhaps augmented, adaptive immune response in CGD. As previous data demonstrated functional NOX2 expression in T cells, our goal here was to determine if NOX2-deficient T cells are inherently altered in their responses. Activation of purified naive CD4(+) T cells from NOX2-deficient mice led to augmented IFN-γ and diminished IL-4 production and an increased ratio of expression of the T(H)1-specific transcription factor T-bet versus the T(H)2-specfic transcription factor GATA-3, consistent with a T(H)1 skewing of naïve T cells. Selective inhibition of TCR-induced STAT5 phosphorylation was identified as a potential mechanism for skewed T helper differentiation. Exposure to antioxidants inhibited, while pro-oxidants augmented T(H)2 cytokine secretion and STAT5 phosphorylation, supporting the redox dependence of these signaling changes. These data suggest that TCR-induced ROS generation from NOX2 activation can regulate the adaptive immune response in a T-cell-inherent fashion, and propose a possible role for redox signaling in T helper differentiation.
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What OpenQuestion holds
Registered trials
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.