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首页> 外文期刊>Cytokine >Interferon gamma induces actin polymerization, Rac1 activation and down regulates phagocytosis in human monocytic cells
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Interferon gamma induces actin polymerization, Rac1 activation and down regulates phagocytosis in human monocytic cells

机译：干扰素γ诱导肌动蛋白聚合，Rac1活化并下调人类单核细胞的吞噬作用

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摘要

IFNγ is a potent activator and IL-10 a powerful inhibitor of macrophage functions. However, neither all cellular functions are enhanced by IFNγ nor IL-10 inhibits all cellular responses. Thus, FcγRs-mediated phagocytosis in monocyte-derived macrophages (MDM) increases after IL-10 treatment, and decreases after treatment with IFNγ, although both IL-10 and IFNγ up regulate FcγRI expression. In this work we investigated the effect of IFNγ and IL-10 on phagocytic signaling by FcγRs in MDM. Treatment with IFNγ diminished phagocytosis of IgG-opsonized SRBC (IgG-SRBC) while treatment with IL-10 increased it. These opposite effects cannot be attributed to changes in FcγR expression induced by each cytokine. Early biochemical responses mediated by FcγRs were distinctly affected by cytokine treatment. Syk phosphorylation and the rise in [Ca 2+] i were higher after IL-10 treatment, whereas IFNγ treatment also increased Syk phosphorylation but had no effect on the rise in [Ca 2+] i. IFNγ treatment led to increased basal levels of F-actin and this effect correlated with the decrease in phagocytosis of both IgG-SRBC and non-opsonized Escherichia coli. IL-10 did not alter F-actin basal levels, and enhanced the phagocytosis of E. coli and IgG-SRBC. The level of F-actin reached after IFNγ treatment was not further increased after stimulation with IgG-SRBC or CCL5, whereas MDM treated with IL-10 showed a slightly higher response than control cells to CCL5. IFNγ increased Rac1-GTP levels. Inhibition of PI3K with LY294002 prevented IFNγ-mediated actin polymerization. Our data suggest that IFNγ induces a higher basal level of F-actin and activation of Rac1, affecting the response to stimuli that induce cytoskeleton rearrangement such as phagocytic or chemotactic stimuli.
机译：IFNγ是有效的激活剂，IL-10是强大的巨噬细胞功能抑制剂。但是，IFNγ不会增强所有细胞功能，IL-10不会抑制所有细胞反应。因此，尽管IL-10和IFNγ都上调了FcγRI的表达，但在IL-10处理后，FcγRs介导的单核细胞巨噬细胞（MDM）中的吞噬作用增加，而在IFNγ处理后减少。在这项工作中，我们研究了IFNγ和IL-10对MDM中FcγRs吞噬信号的影响。 IFNγ处理可减少IgG调理的SRBC（IgG-SRBC）的吞噬作用，而IL-10则可增加吞噬作用。这些相反的作用不能归因于每种细胞因子诱导的FcγR表达的变化。 FcγR介导的早期生化反应受到细胞因子治疗的明显影响。 IL-10处理后，Syk磷酸化和[Ca 2+] i的升高较高，而IFNγ处理也增加了Syk磷酸化，但对[Ca 2+] i的升高没有影响。 IFNγ处理导致F-肌动蛋白的基础水平增加，并且这种作用与IgG-SRBC和非调理大肠杆菌的吞噬作用降低有关。 IL-10不会改变F-肌动蛋白的基础水平，并增强了大肠杆菌和IgG-SRBC的吞噬作用。 IgG-SRBC或CCL5刺激后，IFNγ处理后达到的F-肌动蛋白水平没有进一步提高，而用IL-10处理的MDM对CCL5的反应略高于对照细胞。 IFNγ增加Rac1-GTP水平。 LY294002抑制PI3K可以阻止IFNγ介导的肌动蛋白聚合。我们的数据表明，IFNγ诱导较高水平的F-肌动蛋白和Rac1激活，影响对诱导细胞骨架重排（例如吞噬或趋化性刺激）的刺激的反应。

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