Small anti-viral compounds activate immune cells via the TLR7 MyD88-dependent signaling pathway

被引:1951
作者
Hemmi, H
Kaisho, T
Takeuchi, O
Sato, S
Sanjo, H
Hoshino, K
Horiuchi, T
Tomizawa, H
Takeda, K
Akira, S
机构
[1] Osaka Univ, Microbial Dis Res Inst, Dept Host Def, Suita, Osaka 5650871, Japan
[2] Japan Sci & Technol Corp, Solut Oriented Res Sci & Technol, Suita, Osaka 5650871, Japan
[3] Japan Energy Corp, Pharmaceut & Biotechnol Lab, Toda, Saitama 3358502, Japan
关键词
D O I
10.1038/ni758
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:196 / 200
页数:5
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