Innate Antiviral Responses by Means of TLR7-Mediated Recognition of Single-Stranded RNA

  title={Innate Antiviral Responses by Means of TLR7-Mediated Recognition of Single-Stranded RNA},
  author={Sandra S Diebold and Tsuneyasu Kaisho and Hiroaki Hemmi and Shizuo Akira and Caetano Reis e Sousa},
  pages={1529 - 1531}
Interferons (IFNs) are critical for protection from viral infection, but the pathways linking virus recognition to IFN induction remain poorly understood. Plasmacytoid dendritic cells produce vast amounts of IFN-α in response to the wild-type influenza virus. Here, we show that this requires endosomal recognition of influenza genomic RNA and signaling by means of Toll-like receptor 7 (TLR7) and MyD88. Single-stranded RNA (ssRNA) molecules of nonviral origin also induce TLR7-dependent production… 
Regulation of antiviral innate immune responses by RIG-I family of RNA helicases.
This review describes the distinct mechanisms inducing type I IFNs through Toll-like receptors and RIG-I/MDA5 pathways, which are extracellular or endosomal PRRs for microbial pathogens.
TLR3 Sensing of Viral Infection
The signalling cascades initiated by TLR3 and the modulation of these pathways are reviewed, which stimulate distinct pathways leading to activation of interferon regulatory factor (IRF) and NF- B.
Cutting Edge: Antibody-Mediated TLR7-Dependent Recognition of Viral RNA1
It is shown that Fc receptors mediate the recognition of virus-Ab complexes and that TLR7 is required for human and murine pDC production of cytokines, indicating a role for TLRs in association with Abs in sustaining virus-specific responses.
Interferon Induction by RNA Viruses and Antagonism by Viral Pathogens
This review focuses on the mechanisms of interferon induction and antagonism of the antiviral strategy by RNA viruses.
Toll-like receptors and innate antiviral immunity.
Toll-like receptors (TLRs) participate in the recognition of virus infection, interacting in particular with viral nucleic acids, and trigger type I IFN synthesis.
Antiviral signaling through pattern recognition receptors.
The role of TLRs and RLHs in the antiviral innate immune response is reviewed, located in endosomal compartments, whereas RLH are present in the cytoplasm where they detect viral dsRNA or ssRNA.
Induction of type I interferon by RNA viruses: cellular receptors and their substrates
The roles of TRL3, TLR7/8, retinoic acid inducible gene I, melanoma differentiation-associated gene 5, and the RNA molecules responsible for activating these viral sensors are highlighted.
Toll-Like Receptors and Viruses: Induction of Innate Antiviral Immune Responses
This review will focus on the current knowledge of TLR-mediated immune responses to several viral infections and recently, TLR agonists represent a promising approach for the treatment of infectious diseases.
Innate immune recognition of viral infection
Members of the Toll-like receptor family have emerged as key sensors that recognize viral components such as nucleic acids and induce type I interferon responses via distinct signaling pathways.


Viral infection switches non-plasmacytoid dendritic cells into high interferon producers
The results suggest that multiple dendritic cell types, not just plasmacytoid cells, can act as specialized interferon-producing cells in certain viral infections, and reveal the existence of a TLR-independent pathway for d endritic cell activation that can be the target of viral interference.
Subcellular Localization of Toll-Like Receptor 3 in Human Dendritic Cells 1
Immunoelectron microscopic analysis revealed that TLR3, when stably expressed in the murine B cell line Ba/F3, was specifically accumulated in multivesicular bodies, a subcellular compartment situated in endocytic trafficking pathways, which may reflect participation of cell type-specific multiple pathways in antiviral IFN induction viaTLR3.
Herpes simplex virus type 1 activates murine natural interferon-producing cells through toll-like receptor 9.
Though TLR9/MyD88-deficiency abrogates IPC responses to HSV-1 in vitro, mice lacking either MyD88 orTLR9 are capable of controlling HSV -1 replication in vivo after local infection, demonstrating that TLR 9- and MyD 88-independent pathways in cells other than IPCs can effectively compensate for defective IPC responders.
Toll-like receptors.
The innate immune system in drosophila and mammals senses the invasion of microorganisms using the family of Toll receptors, stimulation of which initiates a range of host defense mechanisms and there is evidence for additional pathways that mediate TLR ligand-specific biological responses.
Activation of influenza virus-specific CD4+ and CD8+ T cells: a new role for plasmacytoid dendritic cells in adaptive immunity.
The results pinpoint a new role of pDCs in the induction of antiviral T-cell responses and suggest that these DCs play a prominent role in the adaptive immune response against viruses.
Antibody-dependent induction of type I interferons by poliovirus in human mononuclear blood cells requires the type II fcgamma receptor (CD32).
It is shown that the IFN-alpha-inducing capacity of attenuated poliovirus vaccine strains is dramatically enhanced in the presence of human polyvalent immunoglobulin G (IgG), and the results suggest that induction of type I interferons by poliov virus-antibody complexes depends on CD32-mediated phagocytosis of RNA-containing viral particles.
Molecular basis for the immunostimulatory activity of guanine nucleoside analogs: Activation of Toll-like receptor 7
  • Jongdae Lee, T. Chuang, H. Cottam
  • Biology, Chemistry
    Proceedings of the National Academy of Sciences of the United States of America
  • 2003
Evidence is presented that guanosine analogs activate immune cells via TLR7 by a pathway that requires endosomal maturation, and the B cell-stimulating and antiviral activities of the guanosin analogs may be explained by theirTLR7-activating capacity.
Plasmacytoid dendritic cells activated by influenza virus and CD40L drive a potent TH1 polarization
It is shown that blood PDCs, when stimulated with influenza virus and CD40L in vitro, undergo a maturation process characterized by up-regulation of major histocompatibility complex proteins and adhesion and costimulatory molecules.