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Positive rates of iNOS (show NOS2 Proteins) in cervical tissues were 72.1%, 28.2%, and 3.1% in the -HPV-positive patients with cervical cancer (CC group), HR-HPV group, and controls, respectively (P < 0.05). Levels of TLR3, TLR4 (show TLR4 Proteins), TLR7 (show TLR7 Proteins), TLR8 (show TLR8 Proteins), NF-kappaB (show NFKB1 Proteins) p65 (show GORASP1 Proteins), and iNOS (show NOS2 Proteins) in cervical epithelial cells were higher in CC group than in other groups.
TLR signaling, in particular TLR3 activation, can efficiently reactivate HIV transcription in infected microglia, but not in monocytes or T cells
This study revealed that TLR2 rs3804100 and TLR3 rs3775291 polymorphisms may be protective factors for HBV-related hepatocellular carcinoma .
TLR3 stimulation induces the Warburg effect in head and neck squamous carcinoma cells in vitro, and suggest that TLR3 may play a role in tumor adaptation to hypoxia.
we report that autophagy is associated with apoptosis processes, involving LC3 (show MAP1LC3A Proteins) and TRIF (show TRIM69 Proteins)-colocation in human HCC (show FAM126A Proteins) cells. Regulation of autophagy and the TLR3-TRIF (show TRIM69 Proteins) pathway may be effective in the treatment of liver cancer.
Polymorphism of CD209 (show CD209 Proteins) and TLR3 genes in populations of North Eurasia
TLR3-activated signaling enhanced the therapeutic effects of human umbilical cord-derived mesenchymal stem cells in a mouse model of colitis
the TLR3 Leu412Phe CC genotype is independently associated with severity of hepatitis C recurrence after LT.
These data demonstrate that in the absence of HBsAg, hepatic hepatitis B virus replication leads to Tlr3-dependent interferon (show IFNA Proteins) responses in non-parenchymal liver cells.
Study found that the astrocytic TLR3-mediated cytokine expression profile is modulated by prostaglandin, and NF-kappaB (show NFKB1 Proteins), ERK1/2 and GSK-3beta are involved in the modulatory mechanism. These results suggest that pathological conditions with increased COX (show COX8A Proteins) activity can neuroimmunologically alter neuron-glia interaction.
TLR3 signaling contributes to Wallerian degeneration after peripheral nerve injury by affecting Schwann cell activation.
This study establishes a correlation between TLR-3 and TLR-9 (show TLR9 Proteins) expression with the development of EAE. In addition, evidence of a role for the myelin peptide in targeting the innate inflammatory response to the CNS is presented.
Data show that HCFC2 (show HCFC2 Proteins) is a critical component of the IRF1 (show IRF1 Proteins) and IRF2 (show IRF2 Proteins) transcriptional machinery that regulates Tlr3 gene expression.
the JAK (show JAK3 Proteins)-STAT (show STAT1 Proteins) pathway provides a cytokine rheostat mechanism, which enables macrophages to fine-tune their responses to multiple, temporally separated infection events involving the TLR3 and TLR7 (show TLR7 Proteins) pathways.
These results suggest that testicular innate immune responses to pathogens caused by nano-TiO2 may be involved in the regulatory mechanisms of TAM (show CCNA1 Proteins)/TLR3 signaling in testicular Sertoli cells.
findings report that RKIP (show PEBP1 Proteins) preferentially regulates the TLR3-mediated immune response in macrophages; phosphorylation of RKIP (show PEBP1 Proteins) serine 109 is required for RKIP (show PEBP1 Proteins) to promote TLR3-mediated signaling and inflammation
Furthermore, Leishmania RNA virus 1-induced TLR-3 activation promoted parasite persistence by enhancing macrophage survival through Akt (show AKT1 Proteins) activation in a manner partially dependent on miR (show MLXIP Proteins)-155.
Primary tumor-derived exosomal RNAs, which are enriched in small nuclear RNAs, activate TLR3 in lung epithelial cells, consequently inducing chemokine (show CCL1 Proteins) secretion in the lung and promoting neutrophil recruitment.
Autophagy contributes to macrophage resistance to Leishmania major. Data, including data from studies in knockout mice, suggest a key resistance mechanism involves endosomal signaling via Tlr3/7/9 in macrophages; macrophages deficient for Tlr3/7/9, Unc93b1, or MyD88 (show MYD88 Proteins) fail to undergo L. major-induced autophagy. (TLR = Toll (show TLR4 Proteins)-like receptor; Unc93b1 = unc-93 homolog B1; MyD88 (show MYD88 Proteins) = myeloid differentiation primary response gene 88 (show MYD88 Proteins))
Our study reveals a novel mechanism of TLR3 in regulation of dendritic morphology and provides an explanation for how environmental factors influence mental health.
These data demonstrated that TLR2, TLR3 and TLR9 (show TLR9 Proteins) contribute to NF-kappaB (show NFKB1 Proteins) activation in response to porcine epidemic diarrhea virus infection, but not RIG-I (show DDX58 Proteins).
TLR3 is regulated differentially by different genotype 1 PRRSV strains and this seems to be related apparently to the replication levels of each strain, as well as, to the TNF-alpha (show TNF Proteins) inducing capability.
5 known non-synonymous single nucleotide polymorphisms (SNPs) were characterized in the coding sequences of the porcine TLR3 gene.
Activation of porcine TLR3 signaling is important in stimulating effective responses to PRRSV infection.
The results from this study demonstrate that expression of at least TLR3, TLR7 (show TLR7 Proteins) and TLR8 (show TLR8 Proteins) is stimulated upon bovine alpha-herpesvirus infection of the brain.
TLR2, 3, 4, and 8 mRNA expression is strongly upregulated and correlates with the progression of atherosclerosis in the aorta. Fluvastatin significantly inhibited this progress and reduced inflammation via TLR downregulation.
18 SNPs of TLR3 were observed and only 4 polymorphic positions were detected in the domestic breeds and 14 non-synonymous substitutions were observed, most of them in the LRR molecules.
Differential gene expression following TLR stimulation in rag1 (show RAG1 Proteins)-/- mutant zebrafish tissues and morphological descriptions of lymphocyte-like cell populations
Binding energy (BE) calculation using MM/PBSA method from the TLR3- and TLR22-ligand complexes revealed an adequate binding affinity between TLR22-monomer and dsRNA as like as TLR3-dimer-dsRNA complex.
Full-length tlr3 was functionally characterized.
The protein encoded by this gene is a member of the Toll-like receptor (TLR) family which plays a fundamental role in pathogen recognition and activation of innate immunity. TLRs are highly conserved from Drosophila to humans and share structural and functional similarities. They recognize pathogen-associated molecular patterns (PAMPs) that are expressed on infectious agents, and mediate the production of cytokines necessary for the development of effective immunity. The various TLRs exhibit different patterns of expression. This receptor is most abundantly expressed in placenta and pancreas, and is restricted to the dendritic subpopulation of the leukocytes. It recognizes dsRNA associated with viral infection, and induces the activation of NF-kappaB and the production of type I interferons. It may thus play a role in host defense against viruses. Use of alternative polyadenylation sites to generate different length transcripts has been noted for this gene.
toll-like receptor 3
, toll-like receptor 3-like
, toll-like receptor 3 variant 1