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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Phosphatidylinositol 3-kinase and extracellular signal-regulated kinase are recruited for Fc receptor-mediated phagocytosis during monocyte-to-macrophage differentiation.
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Phosphatidylinositol 3-kinase and extracellular signal-regulated kinase are recruited for Fc receptor-mediated phagocytosis during monocyte-to-macrophage differentiation.

机译：募集磷脂酰肌醇3-激酶和细胞外信号调节激酶用于单核细胞向巨噬细胞分化过程中Fc受体介导的吞噬作用。

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摘要

The molecular mechanism involved in Fc receptor-mediated phagocytosis in the different cell types of the immune system is still poorly defined. We investigated the role of phosphatidylinositol 3-kinase (PI 3-K) and extracellular signal-regulated kinase (ERK) in phagocytosis by monocytes and by monocyte-differentiated macrophages. Peripheral blood monocytes and monocytic cells (THP-1 cell line) were able to ingest IgG-coated erythrocytes in the absence of additional stimulus. Phagocytosis by these cells was not blocked by wortmannin and LY294002, specific inhibitors of PI 3-K, or by PD98059, a specific MEK/ERK inhibitor. However, upon differentiation of THP-1 monocytes to macrophages, through treatment with retinoic acid and interferon-gamma (IFN-gamma), wortmannin and PD98059 blocked Fc receptor-mediated phagocytosis efficiently. Inhibition of phagocytosis by PD98059 was observed after 24 h of IFN-gamma treatment, whereas wortmannin could inhibit phagocytosis only after 48 h of IFN-gamma treatment. Additionally, phagocytosis of IgG-coated erythrocytes by neutrophils, a more efficient phagocyte, was inhibited by wortmannin and PD98059. Neutrophils and monocyte-differentiated macrophages presented significantly more efficient phagocytosis than monocytes upon PMA stimulation. Taken together, these results indicate that poorly phagocytic leukocytes, such as monocytes, do not require PI 3-K and ERK for phagocytosis. Upon differentiation into macrophages, however, ERK first and PI 3-K second are recruited for regulation of phagocytosis. In addition, our data support the idea that professional phagocytes require ERK and PI 3-K for efficient phagocytosis.
机译：在免疫系统的不同细胞类型中，Fc受体介导的吞噬作用所涉及的分子机制仍不清楚。我们调查了磷脂酰肌醇3-激酶（PI 3-K）和细胞外信号调节激酶（ERK）在单核细胞和单核细胞分化的巨噬细胞吞噬作用中的作用。在没有其他刺激的情况下，外周血单核细胞和单核细胞（THP-1细胞系）能够摄取IgG包被的红细胞。这些细胞的吞噬作用不受PI 3-K的特异性抑制剂渥曼青霉素和LY294002或特异性的MEK / ERK抑制剂PD98059的阻断。然而，在THP-1单核细胞分化为巨噬细胞后，通过视黄酸和干扰素-γ（IFN-γ）处理，渥曼青霉素和PD98059有效地阻断了Fc受体介导的吞噬作用。 IFN-γ处理24小时后，PD98059抑制了吞噬作用，而渥曼青霉素仅在IFN-γ处理48小时后才抑制吞噬作用。另外，渥曼青霉素和PD98059抑制了嗜中性粒细胞（一种更有效的吞噬细胞）对IgG包被的红细胞的吞噬作用。在PMA刺激下，嗜中性粒细胞和单核细胞分化的巨噬细胞比单核细胞具有更高的吞噬效率。综上所述，这些结果表明吞噬能力较差的白细胞，例如单核细胞，不需要PI 3-K和ERK进行吞噬作用。然而，在分化为巨噬细胞后，首先募集了ERK，然后募集了PI 3-K，以调节吞噬作用。此外，我们的数据支持以下观点：专业吞噬细胞需要ERK和PI 3-K才能有效吞噬。

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