| Literature DB >> 11812998 |
Hiroaki Hemmi1, Tsuneyasu Kaisho, Osamu Takeuchi, Shintaro Sato, Hideki Sanjo, Katsuaki Hoshino, Takao Horiuchi, Hideyuki Tomizawa, Kiyoshi Takeda, Shizuo Akira.
Abstract
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.Entities:
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Year: 2002 PMID: 11812998 DOI: 10.1038/ni758
Source DB: PubMed Journal: Nat Immunol ISSN: 1529-2908 Impact factor: 25.606