Small anti-viral compounds activate immune cells via the TLR7 MyD88-dependent signaling pathway
Small anti-viral compounds activate immune cells via the TLR7 MyD88-dependent signaling pathway
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DOI：
10.1038/ni758
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发表时间：
2002-02-01
影响因子：
30.5
通讯作者：
Akira, S
中科院分区：
文献类型：
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作者：
Hemmi, H;Kaisho, T;Akira, S
咪唑并喹啉化合物咪喹莫特和R-848是低分子量免疫应答调节剂，可以诱导多种细胞类型中干扰素α和其他细胞因子的合成。这些化合物具有有效的抗病毒和抗肿瘤特性;然而，它们发挥其抗病毒活性的机制仍不清楚。在这里，我们表明咪唑喹啉通过Toll样受体7（TLR 7）-MyD 88依赖性信号通路激活免疫细胞。在对咪唑并喹啉类药物的反应中，MyD 88和TLR 7缺陷小鼠均未显示出巨噬细胞产生任何炎性细胞因子、脾细胞增殖或树突状细胞成熟。咪唑喹啉诱导的信号传导事件在MyD 88和TLR 7缺陷小鼠中也被消除。
The imidazoquinoline compounds imiquimod and R-848 are low-molecular-weight immune response modifiers that can induce the synthesis of interferon-alpha and other cytokines in a variety of cell types. These compounds have potent anti-viral and anti-tumor properties; however, the mechanisms by which they exert their anti-viral activities remain unclear. Here we show that the imidazoquinolines activate immune cells via the Toll-like receptor 7 (TLR7)-MyD88-dependent signaling pathway. In response to the imidazoquinolines, neither MyD88- nor TLR7-deficient mice showed any inflammatory cytokine production by macrophages, proliferation of splenocytes or maturation of dendritic cells. Imidazoquinoline-induced signaling events were also abolished in both MyD88- and TLR7-deficient mice.