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A protective role in blood vessels has been shown for TLR3 (Toll-like receptor 3), a member of the TLR family of innate immune receptors.
TLR3 plays a vital role in both ZIKV replication.
IFN-beta secretion is through TLR3 and not via TLR4 in HGECs.
the impact of the TLR3 polymorphisms rs3775291 and rs5743305 on the natural course of hepatitis b virus infection, was analysed.
TLR3 stimulation promotes metabolic adaptations likely involved in the mechanisms of disease onset and progression.
This review discusses recent findings on the role of Toll-like receptor 3 (TLR3) deficiencies in the herpes simplex encephalitis development
Intervention of glomerular TLR3 signaling may therefore be a suitable therapeutic strategy for treating glomerulonephritis in the future
The C allele is protective of chronic hepatitis C virus (HCV) infection in TLR3, TLR7 (rs3853839) in females only, and TLR8 (rs3764879) in males only, while risk of infection is linked to the T allele in TLR7 (rs179008) in females only and the A allele in TLR8 (rs3764880) in both sexes.
High TLR3 expression is an independent prognostic factor and has the potential to serve as a clinically useful marker of the need for adjuvant chemotherapy after esophagectomy in patients with advanced thoracic ESCC
Study of TLR3 rs3775290, TLR7 rs17900 and TLR9 rs352140 SNPs in chronic hepatitis C (HCV) Egyptian patient cohort revealed that only heterozygous CT genotype of TLR3 rs3775290 may be a susceptibility risk factor for chronic HCV infection and the homozygous CC and the combined CC-AT-GA female genotypes may be protective.
Results of a study compared Spanish psoriasis patient and healthy controls showed significant associations between functional TLR3, TLR7 and TLR9 single nucleotide polymorphisms and psoriatic arthritis, earlier disease onset and a greater risk for psoriasis.
Single nucleotide polymorphism association analysis showed that the Toll-like receptor 3 (TLR3), prostaglandin-E receptor 3 (PTGER3), and IKZF1 gene were significantly associated with cold medicine-Stevens-Johnson syndrome and toxic epidermal necrolysis with severe ocular complications.
In this study, we provide different lines of evidences demonstrating that dsRNA is a ligand for TLR10 sensing and signaling, and suggest a role of TLR10 as a nucleotide-sensing receptor. We also revealed another function of TLR10, which sequesters dsRNA from TLR3 to regulate IFN signaling.
Cytosolic sensors of viral RNA were found to be involved in IL-6 production via TLR3 signaling in Glomerular Endothelial Cells.
genetic variations in the TLR3 gene could affect the outcome of Hepatitis B Virus infection
Results not only demonstrate the importance of the TLR3 pathway in response to Enterovirus (EV-A71) infection, but also reveal the involvement of EV-A71 protease 2A in subverting TLR3-mediated antiviral defenses.
TLR3 may play a role in the pathogenesis in cervical squamous cell cancer
RIG-I and TLR3 seem to be important factors in the pathogenesis of abdominal aortic aneurysms.
This report present the first detailed investigation of TLR-3 expression in AD brains and show increased levels of TLR-3 mRNA and immunoreactivity, and increased IRF-3 and IFN-beta mRNA expression in Alzheimer's disease.
HIV-1 and TLR3 activation increased endothelial IL6 expression by 6-to-127-fold (P < 0.001), activated c-jun(serine-63) and SAPK/JNK(Thr183/Tyr185).
TLR3 plays a role in modulating epithelial barrier function during Chlamydia infection of epithelial cells lining the genital tract.
TLR3 is required for neonatal heart regeneration and repair after MI. The mechanisms involve glycolytic-dependent YAP1 activation, resulting in miR-152 expression which targets DNMT1/p27kip1.
PolyI:C stimulated BMM of Tlr3(-/-) mice showed a reduction of Ifit1 (p=0.003) and Mx1 (p<0.0001) mRNA compared to control. We here demonstrate that TLR3 can play a protective role in VGD development, possibly regulated via type-I IFNs and a reduced inflammatory response.
TLR3(-/-) and TRIF(-/-) mice presented higher parasite burdens, increased inflammatory lesions, and reduced production of interleukin 12p40, tumor necrosis factor, gamma interferon, and nitric oxide.
TLR3-NFkappaB pathway is necessary for the maturation of committed precursors into mature cardiomyocytes.
The activation of TLR8, TLR7, or TLR3 results in dendritic shortening, and TLR7 and TLR3 but not TLR8 also control axonal growth.
Study found that TLR3 mediates UVB-induced MMP-13 and MMP-3 expressions in mice and may play important role in UVB-induced collagen degradation.
TLR3/TRIF-independent mast cell activation by cytomegalovirus is the dominant mechanism in controlling pulmonary infection.
These data suggest that TLR3 signaling controls the onset and severity of acute pancreatitis.
The results of this study provide evidence that TLR3 plays a critical role in cocaine-induced behavioral effects and further insight into the link between innate immunity and drug dependence.
The TLR3 signaling pathways were activated preferentially in vitro and in vivo and a range of pro-inflammatory cytokines were released following H5N1 infection
up-regulated TLR3 expression and signalling contributes to persistent autophagy following myocardial infarction.
These data indicate that sepsis-induced cardiac dysfunction requires presence of TLR3 and TLR9 and may be linked to histone-induced damage of cardiomyocytes.
Pregnant mice lacking TLR3 in both maternal systemic and placental cells were completely resistant to the hypertension, proteinuria, fetal demise, endothelial dysfunction, splenomegaly, and increases in pro-inflammatory immune cells induced by TLR3 activation.
results indicate that TLR3 is the primary molecule which modulates the activation and function of NK cells during the course of Schistosoma japonicum infection in C57BL/6 mice
This study demonstrates that the synergistic effect between TLR4 and TLR3 in macrophages is an important determinant in acute lung injury and, more importantly, that TLR3 up-regulation is dependent on TLR4-MyD88-NF-kappaB signaling.
Results provide evidence that TLR3 signaling contributes to the dengue virus-induced increase in microglial migration.
this study shows that Tlr3 in nasal CD103(+) dendritic cells is involved in immunoglobulin A production
these data suggest that TLR3 promotes the clearance of Cm during early and mid-stages of genital tract infection, and that loss of TLR3 is detrimental in the development hydrosalpinx.
RIG-I and TLR3 interact with the pseudoknot of Porcine Reproductive and Respiratory Syndrome Virus 3' untranslated regions. Both RIG-I and TLR3 are required for the pseudoknot to induce interferon response.
These data demonstrated that TLR2, TLR3 and TLR9 contribute to NF-kappaB activation in response to porcine epidemic diarrhea virus infection, but not RIG-I.
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 inducing capability.
5 known non-synonymous single nucleotide polymorphisms (SNPs) were characterized in the coding sequences of the porcine TLR3 gene.
molecular sequence characterization and expression in co-infection with influenza virus and Bordetella bronchiseptica
Activation of porcine TLR3 signaling is important in stimulating effective responses to PRRSV infection.
Targeting the Mincle and TLR3 receptor using the dual agonist cationic adjuvant formulation 9 (CAF09) induces humoral and polyfunctional memory T cell responses in calves
On day 104 of pregnancy, mRNA expression of TLRs 3 and 8, as well as that of TLRs 7 and 9, was high in the spleen of fetuses from Neospora caninum-infected heifers. Gene expression levels of endosomal TLRs were also detectable in the placenta and the maternal caruncle from infected heifers, being TLRs 3, 7 and 8 particularly upregulated, mostly in the caruncle.
The results from this study demonstrate that expression of at least TLR3, TLR7 and TLR8 is stimulated upon bovine alpha-herpesvirus infection of the brain.
Comparative sequence analysis revealed a total of 139 polymorphisms, which include single-nucleotide polymorphisms and insertion-deletion polymorphisms.
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-/- 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