Innate Sensing of Viruses by Toll-Like Receptors

Boehme, Karl W.; Compton, Teresa

doi:10.1128/jvi.78.15.7867-7873.2004

Cited by 234 publications

(204 citation statements)

References 83 publications

Supporting

Mentioning

201

Contrasting

Unclassified

Order By: Relevance

“…Toll-like receptors (TLRs) have emerged as important sensors for viral recognition that act as "bridging molecules" between innate and adaptive immunity [1][2][3][4]. TLRs are able to discriminate between different viruses and bacteria by pathogen-associated molecular patterns (PAMPs) and thereby direct a pathogen specific immune response [2,5].…”

Section: Introductionmentioning

confidence: 99%

Associations between SNPs in toll-like receptors and related intracellular signaling molecules and immune responses to measles vaccine: Preliminary results

Dhiman

Ovsyannikova

Vierkant

et al. 2008

Vaccine

139

103

View full text Add to dashboard Cite

Toll-like receptors (TLRs) represent the critical "bridge" between innate and adaptive immunity to viral pathogens. We hypothesized that single nucleotide polymorphisms (SNPs) that potentially influence the expression/function of TLRs and their associated intracellular signaling molecules contribute to variations in humoral and cellular immunity to measles vaccine. We genotyped 190 randomly selected subjects (12-18 years old), previously vaccinated with two doses of measles, for known SNPs in TLR 2, 3, 4, 5, 6, 7, 8 and 9, and their associated intracellular signaling genes. Specific SNPs in the TLR 2, 3, 4, 5, 6, MyD88 and MD2 genes were associated with measles-specific humoral and cellular immunity. Heterozygous variants for rs3775291 (Phe412Leu) and rs5743305 (−926bp in promoter region) of the TLR3 gene were associated with low antibody and lymphoproliferative responses (p ≤ 0.02) to measles vaccination. Heterozygous variants for rs4986790 (Gly299Asp) and rs4986791 (Ile399Thr) in the TLR4 gene demonstrated higher levels of (p ≤ 0.02) IL-4 secretion. Heterozygous variants for SNPs in TLR5 (rs5744174) and TLR6 (rs5743818) were associated with higher levels of (p ≤ 0.02) IFN-γ secretion. In addition, SNPs in MyD88 and MD2, intracellular molecules that associate with TLRs, also demonstrated associations with variations in antibody and IL-10 production (p ≤ 0.03). Thus, we identified specific SNP associations between TLRs and their associated signaling molecules that have a known role in viral immunity and variations in both humoral and cellular immunity following measles vaccination. These data contribute to understanding the immunogenetic mechanisms underlying variations in the immune response to measles vaccine.

show abstract

Section: Introductionmentioning

confidence: 99%

Associations between SNPs in toll-like receptors and related intracellular signaling molecules and immune responses to measles vaccine: Preliminary results

Dhiman

Ovsyannikova

Vierkant

et al. 2008

Vaccine

139

103

View full text Add to dashboard Cite

show abstract

“…The altered expression of TLR3 has been linked to increased responsiveness to viral infection, which was reported in a number of viruses, such as respiratory syncytial virus [4], vaccinia virus [6] and hepatitis C virus (HCV) [12]. Up regulation of TLR3 has also been described for respiratory viruses such as Rhino virus, Influenza virus, and Sendai virus [1,5,7].…”

mentioning

confidence: 99%

Changes in the Cytokine and Toll-Like Receptor Gene Expression Following Infection of Indigenous and Commercial Chickens With Infectious bursal disease virus

et al. 2011

View full text Add to dashboard Cite

A comparative study of cytokine and toll-like receptor (TLR) mRNA expression in 3 weeks old indigenous and commercial chickens infected with a very virulent strain of Infectious bursal disease virus (IBDV) was performed using a custom-made microarray chip. In uninfected indigenous chickens, the basal levels of interleukin (IL) 15 were lower and IL 16 was higher than their commercial counterparts. In the IBDV infected indigenous chickens, only IL16 gene expression was down regulated, while TLR3 expression was up regulated significantly. In the IBDV infected commercial chickens IL15, IL16 and TLR3 were down regulated. But, IL1-b, IL2, IL8, IL12, IL17, interferon (IFN)-a and b were significantly increased compared with the control. In IBDV infected indigenous chickens, IL15, IFN-c, beta-defensin and TLR3 were up regulated compared to virus-infected commercial chickens. The results suggested that up regulation of TLR3, a ligand for double-stranded (ds) RNA probably could account for the possible clinical resistance in these birds. There was a 5.2 fold difference by quantitative real-time RT-PCR between indigenous and commercial chickens in TLR3 mRNA expression. Therefore, TLR3, a receptor for dsRNA could be a putative molecule that could play a role in differential innate and adaptive immune responses to IBDV in commercial and indigenous chickens.

show abstract

“…Host induction of type I IFNs during innate immune responses to antigens, viral, fungal, or bacterial challenge, to single-stranded RNA (ssRNA), double-stranded (dsRNA), and CpG in DNA has been associated with the triggering of a family of receptors termed Toll-like receptors (TLRs) for their sequence similarity to Toll, which was first identified in the fruit fly (reviewed in Boehme and Compton, 2004;Conzelmann, 2005;Kawai and Akira, 2005;Yang et al, 2005). Although many cell types are able to express some TLRs, research has indicated that the plasmacytoid dendritic cell (pDC) maintains a central role in the TLR-triggered IFN response (reviewed in Malmgaard, 2005).…”

Section: Introductionmentioning

confidence: 99%

Peripheral, but not central nervous system, type I interferon expression in mice in response to intranasal vesicular stomatitis virus infection

2007

View full text Add to dashboard Cite

Type I interferon (IFN) is critical for resistance of mice to infection with vesicular stomatitis virus (VSV). Wild type (wt) VSV infection did not induce type I IFN production in vitro or in the central nervous system (CNS) of mice; however IFN-β was detected in lungs, spleen, and serum within 24 h. The M protein mutant VSV, T1026R1 (also referred to as M51R), induced type I IFN production in vitro and in the CNS, with poor expression in spleens. In addition, VSV T1026R1 was not pathogenic to mice after intranasal infection, illustrating the importance of IFN in controlling VSV replication in the CNS. Experiments with chemical sympathectomy, sRAGE, and neutralizing antibody to VSV were performed to investigate the mechanism(s) utilized for induction of peripheral IFN; neither sRAGE infusion nor chemical sympathectomy had an effect on peripheral IFN production. In contrast, administration of neutralizing antibody (Ab) readily blocked the response. Infectious VSV was transiently present in lungs and spleens at 24 h post infection. The results are consistent with VSV traffic from the olfactory neuroepithelium to peripheral lymphoid organs hematogenously or via lymphatic circulation. These results suggest that VSV replicates to high titers in the brains of mice because of the lack of IFN production in the CNS after intranasal VSV infection. In contrast, replication of VSV in peripheral organs is controlled by the production of large amounts of IFN.Address correpondence to

show abstract

Innate Sensing of Viruses by Toll-Like Receptors

Cited by 234 publications

References 83 publications

Associations between SNPs in toll-like receptors and related intracellular signaling molecules and immune responses to measles vaccine: Preliminary results

Associations between SNPs in toll-like receptors and related intracellular signaling molecules and immune responses to measles vaccine: Preliminary results

Changes in the Cytokine and Toll-Like Receptor Gene Expression Following Infection of Indigenous and Commercial Chickens With Infectious bursal disease virus

Peripheral, but not central nervous system, type I interferon expression in mice in response to intranasal vesicular stomatitis virus infection

Contact Info

Product

Resources

About