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Sensing of viral infection and activation of innate immunity by toll-like receptor 3

Elisabeth Vercammen (UGent) , Jens Staal (UGent) and Rudi Beyaert (UGent)
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Organization
Abstract
Toll-like receptors (TLRs) form a major group of transmembrane receptors that are involved in the detection of invading pathogens. Double-stranded RNA is a marker for viral infection that is recognized by TLR3. TLR3 triggering activates specific signaling pathways that culminate in the activation of NF-kappa B and IRF3 transcription factors, as well as apoptosis, enabling the host to mount an effective innate immune response through the induction of cytokines, chemokines, and other proinflammatory mediators. In this review, we describe the paradoxical role of TLR3 in innate immunity against different viruses and in viral pathogenesis but also the evidence for TLR3 as a "danger" receptor in nonviral diseases. We also discuss the structure and cellular localization of TLR3, as well as the complex signaling and regulatory events that contribute to TLR3-mediated immune responses.
Keywords
NF-KAPPA-B, DOUBLE-STRANDED-RNA, IFN-REGULATORY FACTOR-3, HEPATITIS-C VIRUS, INTERFERON-BETA INDUCTION, ADAPTER PROTEIN TRIF, CUTTING EDGE, SIGNALING PATHWAY, TYROSINE RESIDUES, TYPE-2 INFECTION

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Citation

Please use this url to cite or link to this publication:

MLA
Vercammen, Elisabeth, Jens Staal, and Rudi Beyaert. “Sensing of Viral Infection and Activation of Innate Immunity by Toll-like Receptor 3.” CLINICAL MICROBIOLOGY REVIEWS 21.1 (2008): 13–25. Print.
APA
Vercammen, E., Staal, J., & Beyaert, R. (2008). Sensing of viral infection and activation of innate immunity by toll-like receptor 3. CLINICAL MICROBIOLOGY REVIEWS, 21(1), 13–25.
Chicago author-date
Vercammen, Elisabeth, Jens Staal, and Rudi Beyaert. 2008. “Sensing of Viral Infection and Activation of Innate Immunity by Toll-like Receptor 3.” Clinical Microbiology Reviews 21 (1): 13–25.
Chicago author-date (all authors)
Vercammen, Elisabeth, Jens Staal, and Rudi Beyaert. 2008. “Sensing of Viral Infection and Activation of Innate Immunity by Toll-like Receptor 3.” Clinical Microbiology Reviews 21 (1): 13–25.
Vancouver
1.
Vercammen E, Staal J, Beyaert R. Sensing of viral infection and activation of innate immunity by toll-like receptor 3. CLINICAL MICROBIOLOGY REVIEWS. 2008;21(1):13–25.
IEEE
[1]
E. Vercammen, J. Staal, and R. Beyaert, “Sensing of viral infection and activation of innate immunity by toll-like receptor 3,” CLINICAL MICROBIOLOGY REVIEWS, vol. 21, no. 1, pp. 13–25, 2008.
@article{394332,
  abstract     = {Toll-like receptors (TLRs) form a major group of transmembrane receptors that are involved in the detection of invading pathogens. Double-stranded RNA is a marker for viral infection that is recognized by TLR3. TLR3 triggering activates specific signaling pathways that culminate in the activation of NF-kappa B and IRF3 transcription factors, as well as apoptosis, enabling the host to mount an effective innate immune response through the induction of cytokines, chemokines, and other proinflammatory mediators. In this review, we describe the paradoxical role of TLR3 in innate immunity against different viruses and in viral pathogenesis but also the evidence for TLR3 as a "danger" receptor in nonviral diseases. We also discuss the structure and cellular localization of TLR3, as well as the complex signaling and regulatory events that contribute to TLR3-mediated immune responses.},
  author       = {Vercammen, Elisabeth and Staal, Jens and Beyaert, Rudi},
  issn         = {0893-8512},
  journal      = {CLINICAL MICROBIOLOGY REVIEWS},
  keywords     = {NF-KAPPA-B,DOUBLE-STRANDED-RNA,IFN-REGULATORY FACTOR-3,HEPATITIS-C VIRUS,INTERFERON-BETA INDUCTION,ADAPTER PROTEIN TRIF,CUTTING EDGE,SIGNALING PATHWAY,TYROSINE RESIDUES,TYPE-2 INFECTION},
  language     = {eng},
  number       = {1},
  pages        = {13--25},
  title        = {Sensing of viral infection and activation of innate immunity by toll-like receptor 3},
  url          = {http://dx.doi.org/10.1128/CMR.00022-07},
  volume       = {21},
  year         = {2008},
}

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