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维甲酸在耐受和免疫中的作用。

The role of retinoic acid in tolerance and immunity.

机构信息

Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

Immunity. 2011 Jul 22;35(1):13-22. doi: 10.1016/j.immuni.2011.07.002.

DOI:10.1016/j.immuni.2011.07.002
PMID:21777796
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3418663/
Abstract

Vitamin A elicits a broad array of immune responses through its metabolite, retinoic acid (RA). Recent evidence indicates that loss of RA leads to impaired immunity, whereas excess RA can potentially promote inflammatory disorders. In this review, we discuss recent advances showcasing the crucial contributions of RA to both immunological tolerance and the elicitation of adaptive immune responses. Further, we provide a comprehensive overview of the cell types and factors that control the production of RA and discuss how host perturbations may affect the ability of this metabolite to control tolerance and immunity or to instigate pathology.

摘要

维生素 A 通过其代谢产物视黄酸 (RA) 引发广泛的免疫反应。最近的证据表明,RA 的缺失会导致免疫功能受损,而过量的 RA 则可能促进炎症性疾病。在这篇综述中,我们讨论了最近的进展,这些进展展示了 RA 对免疫耐受和适应性免疫反应的产生的重要贡献。此外,我们还全面概述了控制 RA 产生的细胞类型和因素,并讨论了宿主的干扰如何影响这种代谢物控制耐受和免疫的能力,或者引发病理。

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2
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本文引用的文献

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Oral tolerance.口服耐受。
Immunol Rev. 2011 May;241(1):241-59. doi: 10.1111/j.1600-065X.2011.01017.x.
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Prostaglandin E2 suppresses the differentiation of retinoic acid-producing dendritic cells in mice and humans.前列腺素 E2 抑制了小鼠和人类中产生视黄酸的树突状细胞的分化。
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Essential role for retinoic acid in the promotion of CD4(+) T cell effector responses via retinoic acid receptor alpha.视黄酸通过视黄酸受体 α 在促进 CD4(+) T 细胞效应应答中的必需作用。
Front Immunol. 2025 Jul 1;16:1609763. doi: 10.3389/fimmu.2025.1609763. eCollection 2025.
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Effect of prolonged cooking on pro-vitamin A levels of biofortified East African highland bananas.长时间烹饪对生物强化东非高地香蕉中维生素A原水平的影响。
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Comprehensive gene expression analysis of organoid-derived healthy human colonic epithelium and cancer cell line stimulated with live probiotic bacteria.对活益生菌刺激的类器官衍生健康人结肠上皮和癌细胞系进行全面基因表达分析。
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Evaluation of vitamin A levels in patients hospitalized in the general pediatrics unit.对普通儿科病房住院患者维生素A水平的评估。
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Enhancing plasmacytoid dendritic cell functionality with retinoic acid for improved multiple myeloma therapy.用视黄酸增强浆细胞样树突状细胞功能以改善多发性骨髓瘤治疗
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Midkine (MDK) in cancer and drug resistance: from inflammation to therapy.癌症与耐药性中的中期因子(MDK):从炎症到治疗
Discov Oncol. 2025 Jun 11;16(1):1062. doi: 10.1007/s12672-025-02941-1.
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Integrative multi-omics analysis reveals the LncRNA 60967.1-PLCD4-ATRA axis as a key regulator of colorectal cancer progression and immune response.整合多组学分析揭示LncRNA 60967.1-PLCD4-ATRA轴是结直肠癌进展和免疫反应的关键调节因子。
Mol Cancer. 2025 Jun 6;24(1):164. doi: 10.1186/s12943-025-02359-x.
10
Abundance of single filamentous bacteria, and expression of differentiated Th17 cells, their signature cytokine IL-17 A, and retinoic acid receptor are predictive of poor rotavirus vaccine take.单丝状细菌的丰度、分化的Th17细胞的表达、其标志性细胞因子IL-17A以及视黄酸受体可预测轮状病毒疫苗接种效果不佳。
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Immunity. 2011 Mar 25;34(3):435-47. doi: 10.1016/j.immuni.2011.03.003.
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The kinase mTOR regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2.激酶 mTOR 通过选择性激活 mTORC1 和 mTORC2 的信号转导来调节辅助性 T 细胞的分化。
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Functional specialization of interleukin-17 family members.白细胞介素-17 家族成员的功能特化。
Immunity. 2011 Feb 25;34(2):149-62. doi: 10.1016/j.immuni.2011.02.012.
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Intestinal tolerance requires gut homing and expansion of FoxP3+ regulatory T cells in the lamina propria.肠道耐受需要肠道归巢和固有层中 FoxP3+调节性 T 细胞的扩增。
Immunity. 2011 Feb 25;34(2):237-46. doi: 10.1016/j.immuni.2011.01.016. Epub 2011 Feb 17.
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Co-adjuvant effects of retinoic acid and IL-15 induce inflammatory immunity to dietary antigens.维甲酸和白细胞介素-15 的协同作用诱导对膳食抗原的炎症免疫。
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Bile retinoids imprint intestinal CD103+ dendritic cells with the ability to generate gut-tropic T cells.胆酸盐视黄醇可在肠道中 CD103+树突状细胞上留下印迹,使其具有产生肠道归巢 T 细胞的能力。
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Cyp26b1 regulates retinoic acid-dependent signals in T cells and its expression is inhibited by transforming growth factor-β.Cyp26b1 调节 T 细胞中的视黄酸依赖性信号,其表达受转化生长因子-β抑制。
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