Type I interferon (IFN-I) is critical for antiviral defense, and plasmacytoid dendritic cells (pDCs) are a predominant source of IFN-I during virus infection. pDC-mediated antiviral responses are stimulated upon physical contact with infected cells, during which immunostimulatory viral RNA is transferred to pDCs, leading to IFN production via the nucleic acid sensor TLR7.
TIR-TLR7 as a Molecular Adjuvant: Simultaneous Enhancing Humoral and Cell-Mediated Immune Responses Against Inactivated Infectious Bursal Disease Virus.
These findings suggest that a dysfunction of TLR7 in COPD removes the brake on ACh-induced serous secretion during viral infections, resulting in prolonged airway hypersecretion, and that it is one of the triggers of COPD exacerbations.
Earlier, we reported that a toll-like-receptor 7 (TLR7) agonist, resiquimod (R-848), stimulated the systemic immunity when adjuvanted with the inactivated Newcastle disease virus vaccine in the chicken.
Subsequent analysis of these data using modern pathway analysis methods revealed that the TLR7/8 pathway was strongly inhibited in HMC3 cells, while it was activated in JEG-3 cells during virus infection.
We show here that miR-21 is an essential positive regulator for the production of both IFN-α and IFN-λ by pDCs and for promoting host defense against viral infection. miR-21 was markedly upregulated in toll-like receptor (TLR)-activated pDCs and was crucial for TLR7/9 ligand- or herpesvirus-induced production of IFN-α and IFN-λ by pDCs. miR-21-deficient pDCs produced significantly lower levels of IFN-α and IFN-λ on activation than those by wild-type pDCs.
TLR7/9 signals are capable of mounting massive interferon (IFN) response in plasmacytoid dendritic cells (pDCs) immediately after viral infection, yet the involvement of epigenetic regulation in this process has not been documented.
We determined the genotype distribution of single-nucleotide polymorphisms (SNPs) within the TLR3 and TLR7 genes in children with HCMV infection and the relationship between TLR polymorphisms and viral infection.
Inhibition of PP1 activity significantly increases IRF7 phosphorylation and IRF7-mediated IFN-α production in response to Newcastle disease virus (NDV) infection or Toll-like receptor 7 (TLR7) challenge, leading to impaired viral replication.
Our results showed that TLR7 is significantly down-regulated in neoplastic hepatocytes (P < .001), especially in the patients with hepatitis B (n = 52) or C (n = 24) virus infection.
Our results highlight the dual role of TLR7 in immunodeficiency virus infection and vaccination and imply that it may be important to control human AIDS vaccine trials, not only for MHC genotype, but also for TLR7 genotype.
Sensing of viral single-stranded RNA (ssRNA) by Toll-like receptor 7 (TLR7) is likely involved in early pathogen detection and host response to viral infections.
Investigations in mice have demonstrated that the TLR7/9-IFN and TLR3-IFN pathways are different and critical for protective immunity to various experimental viral infections.