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

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.

Pubmed ID: 11812998


  • Hemmi H
  • Kaisho T
  • Takeuchi O
  • Sato S
  • Sanjo H
  • Hoshino K
  • Horiuchi T
  • Tomizawa H
  • Takeda K
  • Akira S


Nature immunology

Publication Data

February 28, 2002

Associated Grants


Mesh Terms

  • Adaptor Proteins, Signal Transducing
  • Adjuvants, Immunologic
  • Aminoquinolines
  • Animals
  • Antigens, Differentiation
  • Antiviral Agents
  • Bone Marrow Cells
  • Dendritic Cells
  • Drosophila Proteins
  • Imidazoles
  • Interferon Inducers
  • Macrophages, Peritoneal
  • Membrane Glycoproteins
  • Mice
  • Mice, Mutant Strains
  • Myeloid Differentiation Factor 88
  • Receptors, Cell Surface
  • Receptors, Immunologic
  • Spleen
  • Toll-Like Receptor 7
  • Toll-Like Receptors