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首页> 外文期刊>Infection and immunity >Induction of gamma interferon production in human alveolar macrophages by Mycobacterium tuberculosis.
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Induction of gamma interferon production in human alveolar macrophages by Mycobacterium tuberculosis.

机译：结核分枝杆菌诱导人肺泡巨噬细胞中γ干扰素的产生。

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Gamma interferon (IFN-gamma) is a cytokine which plays a critical role in resistance to Mycobacterium tuberculosis infection. While T lymphocytes and natural killer cells are a major source of IFN-gamma, previous demonstrations that it can be produced by murine macrophages prompted us to examine the capacity of human alveolar macrophages to express IFN-gamma. Here we report that in vitro infection of alveolar macrophages with M. tuberculosis induces both the release of IFN-gamma protein and a transient increase in IFN-gamma mRNA levels. The IFN-producing cells were shown to be macrophages by reverse transcription-in situ PCR. We also observed that M. tuberculosis stimulation resulted in IFN-gamma-dependent expression of the chemokines IFN-gamma-inducible protein 10 and monokine induced by IFN-gamma, suggesting that macrophage-derived IFN-gamma can function in an autocrine and/or paracrine manner. The existence of a positive regulatory loop was suggested by the observation that exogenous IFN-gamma protein could induce IFN-gamma mRNA expression in uninfected alveolar macrophages. Interleukin-12 was also found to be a potent inducer of IFN-gamma production, and M. tuberculosis-induced IFN-gamma production appears to be mediated, at least in part, by IL-12. In contrast, M. tuberculosis-induced IFN-gamma production by alveolar macrophages could be blocked by exogenous interleukin-10. These studies are the first to demonstrate an autoregulatory role for IFN-gamma produced by alveolar macrophages infected in vitro with M. tuberculosis.
机译：γ干扰素（IFN-γ）是一种细胞因子，在抵抗结核分枝杆菌感染中起关键作用。尽管T淋巴细胞和自然杀伤细胞是IFN-γ的主要来源，但先前的证明它可以由鼠巨噬细胞产生，这使我们研究了人类肺泡巨噬细胞表达IFN-γ的能力。在这里，我们报道结核分枝杆菌在肺泡巨噬细胞的体外感染既诱导IFN-γ蛋白的释放，又引起IFN-γmRNA水平的瞬时增加。通过逆转录-原位PCR显示产生IFN的细胞是巨噬细胞。我们还观察到，结核分枝杆菌刺激导致趋化因子IFN-γ诱导蛋白10和IFN-γ诱导的单因子的IFN-γ依赖性表达，这表明巨噬细胞衍生的IFN-γ可以在自分泌和/或中起作用。旁分泌方式。通过观察发现外源性IFN-γ蛋白可以诱导未感染的肺泡巨噬细胞中IFN-γmRNA表达，表明存在正调节环。还发现白介素-12是IFN-γ产生的有效诱导剂，并且结核分枝杆菌诱导的IFN-γ产生似乎至少部分地由IL-12介导。相比之下，肺泡巨噬细胞由结核分枝杆菌诱导的IFN-γ产生可被外源白介素10阻断。这些研究首次证明了体外感染结核分枝杆菌的肺泡巨噬细胞产生的IFN-γ的自调节作用。

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