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首页> 外文期刊>Cytokine >Interferon-γ, tumor necrosis factor, and interleukin-18 cooperate to control growth of Mycobacterium tuberculosis in human macrophages
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Interferon-γ, tumor necrosis factor, and interleukin-18 cooperate to control growth of Mycobacterium tuberculosis in human macrophages

机译：干扰素-γ，肿瘤坏死因子和白介素18协同控制人类巨噬细胞中结核分枝杆菌的生长

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Mycobacterium tuberculosis (MTB) remains a leading infectious threat to human health. Macrophages are the cells targeted for infection by the bacterium as well as key effector cells for clearance of the pathogen. Interleukin (IL)-27 opposes macrophage-mediated control of MTB because supplying IL-12 and blocking the activity of IL-27 limits bacterial growth in primary human macrophages. The purpose of this study was to determine the immunological regulators of this macrophage mechanism to restrict MTB growth. Interferon (IFN)-γ, TNF-α, and IL-18 were all demonstrated to be important to the environment that limits bacterial growth when IL-12 is supplied and IL-27 is neutralized. We find IL-18 works in conjunction with IL-12 to achieve optimal IFN-γ production in this system. We also demonstrate novel interactions between these cytokines to influence the expression or responsiveness to one another. Quantitative assays show that IFN-γ enhances expression of the IL-18 receptor signaling chain, as well as TNF expression and secretion. In turn, TNF-α augments expression of the receptor for IFN-γ, the amount at the cell surface, and the extent of IFN-γ -induced signaling. We further define how the cytokine environment supports an enhanced state of classical macrophage activation. Collectively, these results describe novel immunological mechanisms that provide additional insights into the effects of IL-12 and IL-27 on macrophage regulation during MTB infection.
机译：结核分枝杆菌（MTB）仍然是对人类健康的主要传染病威胁。巨噬细胞是靶向细菌感染的细胞以及清除病原体的关键效应细胞。白细胞介素（IL）-27反对巨噬细胞介导的MTB的控制，因为供应IL-12和阻断IL-27的活性会限制细菌在原代人类巨噬细胞中的生长。本研究的目的是确定该巨噬细胞机制的免疫调节剂，以限制MTB的生长。当提供IL-12和中和IL-27时，干扰素（IFN）-γ，TNF-α和IL-18都对限制细菌生长的环境很重要。我们发现IL-18与IL-12协同工作可在该系统中实现最佳的IFN-γ产生。我们还展示了这些细胞因子之间的新型相互作用，以影响彼此的表达或响应性。定量分析表明，IFN-γ增强了IL-18受体信号链的表达以及TNF的表达和分泌。继而，TNF-α增加了IFN-γ受体的表达，细胞表面的量以及IFN-γ诱导的信号传导的程度。我们进一步定义了细胞因子环境如何支持经典巨噬细胞激活的增强状态。总的来说，这些结果描述了新颖的免疫学机制，这些机制提供了关于MT-12感染期间IL-12和IL-27对巨噬细胞调节作用的更多见解。

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