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Molecular mechanisms mediating oxidative stress-induced T-cell suppression in cancer

机译:调解氧化应激诱导的癌症T细胞抑制的分子机制

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摘要

In cancer settings, oxidative stress plays an important role in modulation of the immune system. Exposure to reactive oxygen species (ROS), produced by activated granulocytes and macrophages in the context of malignant disorders, causes dysfunction of T-cells and NK cells (Kono et al., 1996a,b; Otsuji et al., 1996; Schmielau and Finn, 2001; Schmielau et al., 2001; Thoren et al., 2007), both being important cell types for tumor defense. Besides local inhibition of T-cells in the vicinity of the tumor, for example due to ROS production by tumor-infiltrating macrophages, production of hydrogen peroxide by activated granulocytes in the circulation leads to systemic T-cell suppression (Schmielau and Finn, 2001). In this overview we focus on recent work describing molecular mechanisms of ROS-mediated T-cell suppression.
机译:在癌症环境中,氧化应激在调节免疫系统中起重要作用。 暴露于通过活性粒细胞和巨噬细胞在恶性疾病的情况下产生的反应性氧物质(ROS)导致T细胞和NK细胞的功能障碍(KONO等,1996A,B; Otsuji等,1996; Schmielau和 FINN,2001; SCHMIELAU等,2001; THOREN等,2007),两者都是肿瘤防御的重要细胞类型。 除局部抑制肿瘤附近的T细胞外,例如由于肿瘤浸润巨噬细胞的ROS产生,通过循环中的活化粒细胞产生过氧化氢导致系统性T细胞抑制(Schmielau和Finn,2001) 。 在这一概述中,我们专注于最近的工作描述ROS介导的T细胞抑制的分子机制。

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