ArticlePloS one2022
Antioxidative enzyme NAD(P)H quinone oxidoreductase 1 (NQO1) modulates the differentiation of Th17 cells by regulating ROS levels.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 26 citations in OpenAlex.
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- The iron metalloproteome of Pseudomonas aeruginosa under oxic and anoxic conditions.Metallomics : integrated biometal science · 2025Article
- The spatiotemporal heterogeneity of reactive oxygen species in the malignant transformation of viral hepatitis to hepatocellular carcinoma: a new insight.Cellular & molecular biology letters · 2025Review
- Effect of Ultra-High Pressure on the Extraction of the Free, Esterified, and Bound Phenolics fromMolecules (Basel, Switzerland) · 2025Article
- Effects of 3-(4-Hydroxy-3-methoxyphenyl)propionic Acid on Regulating Oxidative Stress and Muscle Fiber Composition.Nutrients · 2025Article
- Structure characterization of Grifola frondosa polysaccharide and its effect on insulin resistance in HFD-fed mice.NPJ science of food · 2025Article
- Review
- HScience advances · 2024Article
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- Pan-cancer and single-cell analysis reveal the prognostic value and immune response of NQO1.Frontiers in cell and developmental biology · 2023Article
- CT radiomics for noninvasively predicting NQO1 expression levels in hepatocellular carcinoma.PloS one · 2023Article
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Authors and funding
5 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
NAD(P)H quinone oxidoreductase 1 (NQO1) is a flavoprotein that catalyzes two-electron reduction of quinone to hydroquinone by using nicotinamide adenine dinucleotide (NADPH), and functions as a scavenger for reactive oxygen species (ROS). The function of NQO1 in the immune response is not well known. In the present study, we demonstrated that Nqo1-deficient T cells exhibited reduced induction of T helper 17 cells (Th17) in vitro during Th17(23)- and Th17(β)- skewing conditions. Nqo1-deficient mice showed ameliorated symptoms in a Th17-dependent autoimmune Experimental autoimmune encephalomyelitis (EAE) model. Impaired Th17-differentiation was caused by overproduction of the immunosuppressive cytokine, IL-10. Increased IL-10 production in Nqo1-deficient Th17 cells was associated with elevated intracellular Reactive oxygen species (ROS) levels. Furthermore, overproduction of IL-10 in Th17 (β) cells was responsible for the ROS-dependent increase of c-avian musculoaponeurotic fibrosarcoma (c-maf) expression, despite the lack of dependency of c-maf in Th17(23) cells. Taken together, the results reveal a novel role of NQO1 in promoting Th17 development through the suppression of ROS mediated IL-10 production.
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