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吲哚胺2,3-双加氧酶在肝损伤中免疫作用的新角色

Emerging Roles on Immunological Effect of Indoleamine 2,3-Dioxygenase in Liver Injuries.

作者信息

Xu Lingyan, Ling Jiawei, Su Chang, Su Yu-Wen, Xu Yan, Jiang Zhenzhou

机构信息

Sir Run Run Hospital, Nanjing Medical University, Nanjing, China.

Institute of Chinese Medicine and State Key Laboratory of Research on Bioactivities and Clinical Applications of Medicinal Plants, The Chinese University of Hong Kong, Hong Kong, China.

出版信息

Front Med (Lausanne). 2021 Nov 18;8:756435. doi: 10.3389/fmed.2021.756435. eCollection 2021.

DOI:10.3389/fmed.2021.756435
PMID:34869457
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8636938/
Abstract

Indoleamine 2,3-dioxygenase (IDO) is one of the initial rate-limiting enzymes of the kynurenine pathway (KP), which causes immune suppression and induction of T cell anergy. It is associated with the imbalance of immune homeostasis in numerous diseases including cancer, chronic viral infection, allergy, and autoimmune diseases. Recently, IDO has extended its role to liver field. In this review, we summarize the dysregulation and potentials of IDO in the emerging field of liver injuries, as well as current challenges for IDO targets. In particular, we discuss unexpected conclusions against previous work published. IDO is induced by pro-inflammatory cytokines in liver dysfunction and exerts an immunosuppressive effect, whereas the improvement of liver injury may require consideration of multiple factors besides IDO.

摘要

吲哚胺2,3-双加氧酶(IDO)是犬尿氨酸途径(KP)的初始限速酶之一,该途径会导致免疫抑制和T细胞无反应性的诱导。它与包括癌症、慢性病毒感染、过敏和自身免疫性疾病在内的多种疾病中的免疫稳态失衡有关。最近,IDO在肝脏领域的作用得到了扩展。在本综述中,我们总结了IDO在肝损伤这一新兴领域中的失调情况和潜力,以及针对IDO靶点目前面临的挑战。特别是,我们讨论了与之前发表的工作相悖的意外结论。IDO在肝功能障碍中由促炎细胞因子诱导产生,并发挥免疫抑制作用,而肝损伤的改善可能需要考虑除IDO之外的多种因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5380/8636938/f7ba88d9fd3c/fmed-08-756435-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5380/8636938/e585511f1c07/fmed-08-756435-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5380/8636938/f7ba88d9fd3c/fmed-08-756435-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5380/8636938/e585511f1c07/fmed-08-756435-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5380/8636938/f7ba88d9fd3c/fmed-08-756435-g0002.jpg

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FEBS J. 2022 Oct;289(20):6099-6118. doi: 10.1111/febs.16086. Epub 2021 Jun 30.
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Front Pharmacol. 2021 May 6;12:681320. doi: 10.3389/fphar.2021.681320. eCollection 2021.
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Cancer Associated Fibroblasts Promote Renal Cancer Progression Through a TDO/Kyn/AhR Dependent Signaling Pathway.
Biomedicines. 2023 Jul 13;11(7):1988. doi: 10.3390/biomedicines11071988.
癌症相关成纤维细胞通过TDO/犬尿氨酸/芳香烃受体依赖的信号通路促进肾癌进展。
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Pharmacol Ther. 2021 Sep;225:107845. doi: 10.1016/j.pharmthera.2021.107845. Epub 2021 Apr 5.
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