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抗氧化酶 NAD(P)H 醌氧化还原酶 1 (NQO1) 通过调节 ROS 水平调节 Th17 细胞的分化。

Antioxidative enzyme NAD(P)H quinone oxidoreductase 1 (NQO1) modulates the differentiation of Th17 cells by regulating ROS levels.

机构信息

Department of Immunology and Pathology, Research Center for Hepatitis and Immunology, Research Institute, National Center for Global Health and Medicine, Ichikawa-shi, Chiba, Japan.

Department of Immunology, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.

出版信息

PLoS One. 2022 Jul 29;17(7):e0272090. doi: 10.1371/journal.pone.0272090. eCollection 2022.

DOI:10.1371/journal.pone.0272090
PMID:35905076
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9337673/
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.

摘要

烟酰胺腺嘌呤二核苷酸（NAD(P)H）醌氧化还原酶 1（NQO1）是一种黄素蛋白，可通过使用烟酰胺腺嘌呤二核苷酸（NADPH）将醌催化还原为氢醌，并作为活性氧（ROS）的清除剂。NQO1 在免疫反应中的功能尚不清楚。在本研究中，我们证明了 Nqo1 缺陷型 T 细胞在 Th17(23)-和 Th17(β)-偏向条件下体外诱导 Th17 细胞的能力降低。Nqo1 缺陷型小鼠在 Th17 依赖性自身免疫性实验性自身免疫性脑脊髓炎（EAE）模型中症状改善。Th17 分化受损是由于免疫抑制细胞因子 IL-10 的过度产生所致。Nqo1 缺陷型 Th17 细胞中 IL-10 的过度产生与细胞内活性氧（ROS）水平的升高有关。此外，Th17(β)细胞中 IL-10 的过度产生导致 c-禽肌筋膜纤维肉瘤（c-maf）表达的 ROS 依赖性增加，尽管 Th17(23)细胞中 c-maf 的依赖性缺乏。总之，这些结果揭示了 NQO1 通过抑制 ROS 介导的 IL-10 产生来促进 Th17 发育的新作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cbd/9337673/133c888a84ba/pone.0272090.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cbd/9337673/ee22124c3fad/pone.0272090.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cbd/9337673/09de51d2d32f/pone.0272090.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cbd/9337673/1baaea1a639c/pone.0272090.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cbd/9337673/16e4ac510c31/pone.0272090.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cbd/9337673/133c888a84ba/pone.0272090.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cbd/9337673/ee22124c3fad/pone.0272090.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cbd/9337673/09de51d2d32f/pone.0272090.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cbd/9337673/1baaea1a639c/pone.0272090.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cbd/9337673/16e4ac510c31/pone.0272090.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cbd/9337673/133c888a84ba/pone.0272090.g005.jpg

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