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Impact of Interleukin-17 on Macrophage Phagocytosis of Apoptotic Neutrophils and Particles

机译:白细胞介素17对凋亡中性粒细胞和颗粒巨噬细胞吞噬的影响

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摘要

There is now substantial evidence that the cytokine interleukin-17 orchestrates the accumulation of neutrophils in mammals and thereby contributes to host defense. However, the role of IL-17 in controlling neutrophil turnover is not fully understood. Here, we demonstrate that IL-17 stimulates the apoptosis of mouse neutrophils and, simultaneously, the release of the microbicidal compound, myeloperoxidase. IL-17 also stimulates mouse macrophages to phagocytose aged neutrophils and latex beads, and it induces an increase in a soluble form of the phagocytic receptor, lectin-like oxidized low-density lipoprotein receptor-1 as well. In contrast, IL-17 does not markedly increase the release of the archetype neutrophil-recruiting cytokine, macrophage inflammatory protein-2 in mouse macrophages. Importantly, IL-17 also stimulates the phagocytosis of latex beads in human monocyte-derived macrophages. Thus, IL-17 bears the potential to control both phagocytosis and neutrophil turnover during activation of host defense.
机译:现在有大量证据表明,细胞因子白介素17可以协调哺乳动物中嗜中性粒细胞的积累,从而有助于宿主防御。但是,IL-17在控制中性粒细胞更新中的作用尚不完全清楚。在这里,我们证明IL-17刺激小鼠嗜中性白细胞的凋亡,同时释放杀微生物化合物髓过氧化物酶。 IL-17还刺激小鼠巨噬细胞吞噬老化的嗜中性粒细胞和乳胶珠,并诱导吞噬受体,凝集素样氧化型低密度脂蛋白受体-1的可溶性形式增加。相反,IL-17在小鼠巨噬细胞中并未显着增加原型中性粒细胞募集细胞因子巨噬细胞炎性蛋白2的释放。重要的是,IL-17还刺激人单核细胞衍生的巨噬细胞中乳胶珠的吞噬作用。因此,IL-17具有在宿主防御激活期间控制吞噬作用和嗜中性白细胞更新的潜力。

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