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Data suggest that, unlike non-metastatic intestinal epithelial cells (IECs), metastatic IECs express TLR3 and that TLR3 agonists induce inflammatory cytokine (CXCL10 (show CXCL10 Proteins)) production and promote invasiveness of IECs. (TLR3 = toll-like receptor 3; CXCL10 (show CXCL10 Proteins) = chemokine (show CCL1 Proteins) [C-X-C motif] ligand 10 protein)
TLR3-activated macrophages release exosomes that contain anti-HCV microRNA (miRNA)-29 family member
homozygous IFITM3 (show IFITM3 Proteins) CC and TLR3 CC genotypes showed significant independent associations with higher death risks in H7N9/H1N1pdm09 influenza in a large Chinese cohort
TLR3 activation can induce metabolic reprogramming in a pharyngeal cancer cell line, leading to increased aerobic glycolysis, cell migration, elevated levels of reactive oxidative species (ROS (show ROS1 Proteins)), and decreased anti-oxidative response.
Ligand-driven triggering of TLR-3, -4, NOD2, and DC-SIGN (show CD209 Proteins), despite reducing viral replication, markedly increased the capacity of infected dendritic cells to stimulate HIV-specific cytotoxic T-cells.
Since mumps virus SH coimmunoprecipitated with tumor necrosis factor receptor 1 (TNFR1 (show TNFRSF1A Proteins)), RIP1 (show UQCRFS1 Proteins), and IRAK1 (show IRAK1 Proteins), we hypothesize that SH exerts its NF-kappaB (show NFKB1 Proteins) activation inhibitory function by interacting with TNFR1 (show TNFRSF1A Proteins), interleukin-1 receptor type 1 (IL-1R1), and TLR3 complexes in the plasma membrane of infected cells.
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.
the L412F polymorphism in the TLR3 gene could be a genetic risk factor for the development of human cytomegalovirus disease
Studied Toll-like receptor 3 (TLR3) mutations in a cohort of 11 adult Italian viral encephalitis patients.
Report PD-1 (show PDCD1 Proteins)/PD-L1 (show CD274 Proteins) and TLR3 expression in malignant pleural mesotheliomas as possible tests for selection patients who could benefit from immunotherapy.
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.
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.
LUBAC components control TLR3-mediated innate immunity, thereby preventing development of immunodeficiency and autoinflammation.
results reveal a novel CD40 (show CD40 Proteins)-dependent regulation of PD-L1 (show CD274 Proteins) trafficking induced upon TLR3 signaling that dictates its inhibitory activity.
This study reveals novel insights into the pathophysiology of epilepsy and the contribution of TLR3 to disease progression.
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