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the current study shows that motolimod ( selective small-molecule agonist of TLR8, stimulates natural killer (NK) cells, dendritic cells, and monocytes))can be safely administered in combination with cetuximab with an acceptable toxicity profile
TLR7 (show TLR7 Proteins) and TLR8 genetic polymorphisms are associated with susceptibility to mycobacterium tuberculosis infection, and the link is shaped by less effective MTB (show NCAPG2 Proteins) phagocytosis and impaired TLR signaling.
Epstein-Barr virus (EBV) replication activating the toll like receptor 8 (TLR8) molecular pathway in primary monocytes.
Inhibition of Snapin (show SNAPIN Proteins) enhanced localization of HIV-1 with TLR8(+) early endosomes, triggered a pro-inflammatory response, and inhibited trans-infection of CD4 (show CD4 Proteins)(+) T cells.
Study evaluated innate immune profiles following TLR stimulation in HIV-1-infected mothers and newborns, found significantly compromised cytokine responses upon extracellular and intracellular TLR activation. Myeloid dendritic cell (DC) responsiveness appeared to be less impaired than plasmacytoid DCs, and might be enhanced through TLR7 (show TLR7 Proteins)/TLR8 activation.
This is the first study illustrating certain genotypes of TLR-7 (show TLR7 Proteins) and TLR-8 single nucleotide polymorphisms viz. CT(p = 0.002)]; rs3853839[GC(p < 0.001), CC(p = 0.039)] and rs3764879[GC(p < 0.001)] were considerably associated with Chikungunya virus susceptibility.
Data indicate a mechanism in which Toll (show TLR4 Proteins)-like receptors TLR7 (show TLR7 Proteins)/8 signaling, through shedding of FcgRIIA, shifts neutrophil function from phagocytosis to a programmed necrosis pathway, neutrophil extracellular trap formation (NETosis).
this study identified TLR8 as mediator of monocyte differentiation and M2 macrophage polarization during hepatitis C virus infection
COPD (show ARCN1 Proteins) lung tissue explants showed a greater pro-inflammatory response to TLR3 (show TLR3 Proteins) or TLR7 (show TLR7 Proteins)/8 activation than control smokers.
combination adjuvant systems demonstrate markedly different immune activation with age, with combined DC activation via Macrophage-inducible C-type lectin (show CLEC4E Proteins) and TLR7 (show TLR7 Proteins)/8 representing a novel approach to enhance the efficacy of early-life vaccines.
Evaluation of the adjuvant effect of agonists of toll-like receptor 4 (show TLR4 Proteins) and 7/8 in a vaccine against leishmaniasis
TLR8 coupling with SOCS-1 (show SOCS1 Proteins) inhibits TLR7 (show TLR7 Proteins)-mediated antiviral immunity during WNV infection in mice.
this study shows that beta,beta-dimethylacryloyl alkannin could inhibit psoriasis-activated dendritic cells via the TLR7 (show TLR7 Proteins)/8 pathway
an important role of 2'-O-methylation for shaping differential TLR7 (show TLR7 Proteins) or TLR8 activation
Hepatic expression of Tlr6 (show TLR6 Proteins), but not that of Tlr8 is epigenetically controlled, and that the dysregulations of Tlr6 (show TLR6 Proteins) and Tlr8 critically contribute to Testosterone (T)-induced persistent susceptibility to P. chabaudi malaria.
The urinary levels of Tlr8 mRNA were also higher in BXSB-Yaa mice.
TLR8 deletion accelerated autoimmunity in lupus-prone mice in response to TLR7 (show TLR7 Proteins) activation.
TLR8 activation has direct anti-leukemic effects independent of its immunomodulating properties.
We suggest that giant cell formation may be a unique feature of TLR9 (show TLR9 Proteins)- and TLR7 (show TLR7 Proteins)/8-mediated macrophage activation.
These results suggest that IL-23 (show IL23A Proteins)-driven inflammation in mouse skin may be dependent on signaling mediated by TLRs 7, 8, and 9
The results from this study demonstrate that expression of at least TLR3 (show TLR3 Proteins), TLR7 (show TLR7 Proteins) and TLR8 is stimulated upon bovine alpha-herpesvirus infection of the brain.
Knockdown TLR8 increased the apoptosis induced by Bacillus Calmette Guerin infection, and this enhanced apoptosis was caspase (show CASP3 Proteins)-dependent.
A five-amino-acid motif in the undefined region of the TLR8 ectodomain is required for species-specific ligand recognition.
a ligand-induced dimer conformational switch is mainly responsible for TLR8 activation.
multiple regions, including ECD (show ECD Proteins), TM, linker and TIR-tail regions of bTLR8, are involved in determining the localization of cellular ER compartment.
Porcine TLR7 (show TLR7 Proteins) and TLR8 genes from pig lymph node tissue, were cloned and characterized.
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.
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 gene is predominantly expressed in lung and peripheral blood leukocytes, and lies in close proximity to another family member, TLR7, on chromosome X.