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Impaired NK cells' activity and increased numbers of CD4+CD25+regulatory T cells in multidrug-resistant Mycobacterium tuberculosis patients

机译:耐多药结核分枝杆菌患者NK细胞活性受损和CD4 + CD25 +调节性T细胞数量增加

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Multidrug-resistant tuberculosis (MDR-TB) often causes persistent infection and chemotherapy failure, which brings heavy burden of society and family. Many immune cell subsets and regulatory mechanisms may operate throughout the various stages of infection. The presence of regulatory T cells (Tregs) is thought to be an important mechanism that TB successfully evades the immune system. Tregs play a central role in the prevention of autoimmunity and in the control of immune responses. The role of Tregs in MDR-TB infection and persistence is inadequately documented. The current study was designed to determine whether CD4 + CD25+ regulatory T cells may modulate innate immunity (such as NK cells) against human tuberculosis. Our results indicated that the numbers of CD4 + CD25+ Treg cells increased in MDR-TB patients' blood, and the cytokine production of IL-10 increased from MDR-patients compared with healthy subjects, along with the lower activity and low CD69 expression of NK cells in patients. These results suggested that immunity to MDR-TB patients induced circulating CD4 + CD25+ T regulatory cells expansion, which may be related to the persistence of Mycobacterium tuberculosis (M. tb) infection, and to the balance between effectors immune responses and suppression immune responses. (C) 2016 Elsevier Ltd. All rights reserved.
机译:耐多药结核病(MDR-TB)经常引起持续感染和化疗失败,给社会和家庭带来沉重负担。许多免疫细胞亚群和调节机制可能贯穿感染的各个阶段。调节性T细胞(Tregs)的存在被认为是TB成功逃避免疫系统的重要机制。 Treg在预防自身免疫和控制免疫反应中起着核心作用。 Tregs在耐多药结核病感染和持久性中的作用没有足够的文献记载。当前的研究旨在确定CD4 + CD25 +调节性T细胞是否可以调节针对人类结核病的先天免疫力(例如NK细胞)。我们的结果表明,与健康受试者相比,耐多药结核病患者血液中CD4 + CD25 + Treg细胞的数量增加,耐多药患者中IL-10的细胞因子产生增加,并且NK的活性较低且CD69表达较低患者体内的细胞。这些结果表明,对耐多药结核病患者的免疫诱导了循环中的CD4 + CD25 + T调节性细胞扩增,这可能与结核分枝杆菌(M. tb)感染的持续存在以及效应子免疫反应和抑制性免疫反应之间的平衡有关。 (C)2016 Elsevier Ltd.保留所有权利。

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