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白细胞介素-17介导的诱导型一氧化氮合酶激活

Inducible nitric oxide synthase activation by interleukin-17.

作者信息

Miljkovic Djordje, Trajkovic Vladimir

机构信息

Institute for Biological Research, Belgrade, Serbia and Montenegro.

出版信息

Cytokine Growth Factor Rev. 2004 Feb;15(1):21-32. doi: 10.1016/j.cytogfr.2003.10.003.

Abstract

Interleukin-17 (IL-17) is a proinflammatory T cell cytokine presumably involved in physiological responses to infection, but also in immunopathology of autoimmune disorders such as rheumatoid arthritis. The proinflammatory action of IL-17 depends considerably on its ability to trigger the expression of inducible nitric oxide (NO) synthase (iNOS), an enzyme responsible for the generation of cytotoxic and immunoregulatory free radical NO. Here we discuss the role of IL-17 in the cytokine network controlling iNOS expression, and analyze signaling pathways employed by IL-17 for the initiation of iNOS gene transcription. We also propose biological consequences of IL-17-mediated NO release that could be relevant for the mechanisms or therapy of autoimmune and inflammatory disorders.

摘要

白细胞介素-17(IL-17)是一种促炎性T细胞细胞因子,可能参与对感染的生理反应,也参与类风湿性关节炎等自身免疫性疾病的免疫病理学过程。IL-17的促炎作用在很大程度上取决于其触发诱导型一氧化氮(NO)合酶(iNOS)表达的能力,iNOS是一种负责产生具有细胞毒性和免疫调节作用的自由基NO的酶。在此,我们讨论IL-17在控制iNOS表达的细胞因子网络中的作用,并分析IL-17用于启动iNOS基因转录的信号通路。我们还提出了IL-17介导的NO释放可能与自身免疫性疾病和炎症性疾病的机制或治疗相关的生物学后果。

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