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Antioxidative enzyme NAD(P)H quinone oxidoreductase 1 (NQO1) modulates the differentiation of Th17 cells by regulating ROS levels
by
Takahashi, Satoru
, Nishida-Tamehiro, Kyoko
, Tsubata, Takeshi
, Kimura, Akihiro
, Suzuki, Harumi
in
Adenine
/ Animals
/ Antioxidants
/ Biology and Life Sciences
/ c-Maf protein
/ Cell culture
/ Cell differentiation
/ Cytokines
/ Differentiation
/ Disease
/ Enzymes
/ Experimental allergic encephalomyelitis
/ Experiments
/ Fibrosarcoma
/ Helper cells
/ Hydroquinone
/ Immune response
/ Immune system
/ Interleukin 10
/ Lymphocytes
/ Lymphocytes T
/ Medicine and Health Sciences
/ Metabolism
/ Mice
/ NAD
/ NAD(P)H Dehydrogenase (Quinone) - genetics
/ NAD(P)H Dehydrogenase (Quinone) - metabolism
/ NADH, NADPH Oxidoreductases
/ NADPH
/ NADPH quinone oxidoreductase
/ Nicotinamide
/ Nicotinamide adenine dinucleotide
/ Oxidoreductase
/ Oxygen
/ Paralysis
/ Pathogenesis
/ Physical Sciences
/ Quinone oxidoreductase
/ Quinones
/ Reactive oxygen species
/ Reactive Oxygen Species - metabolism
/ Research and Analysis Methods
/ Signal transduction
/ T cell receptors
/ Th17 Cells - metabolism
/ Transcription factors
2022
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Antioxidative enzyme NAD(P)H quinone oxidoreductase 1 (NQO1) modulates the differentiation of Th17 cells by regulating ROS levels
by
Takahashi, Satoru
, Nishida-Tamehiro, Kyoko
, Tsubata, Takeshi
, Kimura, Akihiro
, Suzuki, Harumi
in
Adenine
/ Animals
/ Antioxidants
/ Biology and Life Sciences
/ c-Maf protein
/ Cell culture
/ Cell differentiation
/ Cytokines
/ Differentiation
/ Disease
/ Enzymes
/ Experimental allergic encephalomyelitis
/ Experiments
/ Fibrosarcoma
/ Helper cells
/ Hydroquinone
/ Immune response
/ Immune system
/ Interleukin 10
/ Lymphocytes
/ Lymphocytes T
/ Medicine and Health Sciences
/ Metabolism
/ Mice
/ NAD
/ NAD(P)H Dehydrogenase (Quinone) - genetics
/ NAD(P)H Dehydrogenase (Quinone) - metabolism
/ NADH, NADPH Oxidoreductases
/ NADPH
/ NADPH quinone oxidoreductase
/ Nicotinamide
/ Nicotinamide adenine dinucleotide
/ Oxidoreductase
/ Oxygen
/ Paralysis
/ Pathogenesis
/ Physical Sciences
/ Quinone oxidoreductase
/ Quinones
/ Reactive oxygen species
/ Reactive Oxygen Species - metabolism
/ Research and Analysis Methods
/ Signal transduction
/ T cell receptors
/ Th17 Cells - metabolism
/ Transcription factors
2022
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Antioxidative enzyme NAD(P)H quinone oxidoreductase 1 (NQO1) modulates the differentiation of Th17 cells by regulating ROS levels
by
Takahashi, Satoru
, Nishida-Tamehiro, Kyoko
, Tsubata, Takeshi
, Kimura, Akihiro
, Suzuki, Harumi
in
Adenine
/ Animals
/ Antioxidants
/ Biology and Life Sciences
/ c-Maf protein
/ Cell culture
/ Cell differentiation
/ Cytokines
/ Differentiation
/ Disease
/ Enzymes
/ Experimental allergic encephalomyelitis
/ Experiments
/ Fibrosarcoma
/ Helper cells
/ Hydroquinone
/ Immune response
/ Immune system
/ Interleukin 10
/ Lymphocytes
/ Lymphocytes T
/ Medicine and Health Sciences
/ Metabolism
/ Mice
/ NAD
/ NAD(P)H Dehydrogenase (Quinone) - genetics
/ NAD(P)H Dehydrogenase (Quinone) - metabolism
/ NADH, NADPH Oxidoreductases
/ NADPH
/ NADPH quinone oxidoreductase
/ Nicotinamide
/ Nicotinamide adenine dinucleotide
/ Oxidoreductase
/ Oxygen
/ Paralysis
/ Pathogenesis
/ Physical Sciences
/ Quinone oxidoreductase
/ Quinones
/ Reactive oxygen species
/ Reactive Oxygen Species - metabolism
/ Research and Analysis Methods
/ Signal transduction
/ T cell receptors
/ Th17 Cells - metabolism
/ Transcription factors
2022
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Antioxidative enzyme NAD(P)H quinone oxidoreductase 1 (NQO1) modulates the differentiation of Th17 cells by regulating ROS levels
Journal Article
Antioxidative enzyme NAD(P)H quinone oxidoreductase 1 (NQO1) modulates the differentiation of Th17 cells by regulating ROS levels
2022
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Overview
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.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Animals
/ Disease
/ Enzymes
/ Experimental allergic encephalomyelitis
/ Medicine and Health Sciences
/ Mice
/ NAD
/ NAD(P)H Dehydrogenase (Quinone) - genetics
/ NAD(P)H Dehydrogenase (Quinone) - metabolism
/ NADPH
/ NADPH quinone oxidoreductase
/ Nicotinamide adenine dinucleotide
/ Oxygen
/ Quinones
/ Reactive Oxygen Species - metabolism
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