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Human Monoclonal TLR8 Primary Antibody for CyTOF, FACS - ABIN4360386
Dasari, Zola, Nicholson: Expression of Toll-like receptors by neonatal leukocytes. in Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology 2011
Show all 41 Pubmed References
Human Monoclonal TLR8 Primary Antibody for FACS - ABIN4360384
Wang, Eng, Lin, Liu, Chang, Lin: Functional polymorphisms of TLR8 are associated with hepatitis C virus infection. in Immunology 2014
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Human Monoclonal TLR8 Primary Antibody for ELISA - ABIN4248154
Kaji, Tanaka, Sugita, Kato, Ibata, Shono, Ohta, Kondo, Asaka, Imamura: Ciprofloxacin inhibits lipopolysaccharide-induced toll-like receptor-4 and 8 expression on human monocytes derived from adult and cord blood. in Annals of hematology 2008
Show all 21 Pubmed References
Human Monoclonal TLR8 Primary Antibody for FACS, IHC (p) - ABIN531990
Hart, Athie-Morales, OConnor, Gardiner: TLR7/8-mediated activation of human NK cells results in accessory cell-dependent IFN-gamma production. in Journal of immunology (Baltimore, Md. : 1950) 2005
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Human Monoclonal TLR8 Primary Antibody for FACS - ABIN786836
Itoh, Tatematsu, Watanabe, Iwano, Funami, Seya, Matsumoto: UNC93B1 physically associates with human TLR8 and regulates TLR8-mediated signaling. in PLoS ONE 2011
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Human Monoclonal TLR8 Primary Antibody for IHC (fro), FACS - ABIN786835
Todt, Freeman, Brown, Sonstein, Ames, McCubbrey, Martinez, Chensue, Beck, Curtis: Smoking decreases the response of human lung macrophages to double-stranded RNA by reducing TLR3 expression. in Respiratory research 2013
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Human Monoclonal TLR8 Primary Antibody for ELISA, WB - ABIN526632
Cervantes, Dunham-Ems, La Vake, Petzke, Sahay, Sellati, Radolf, Salazar: Phagosomal signaling by Borrelia burgdorferi in human monocytes involves Toll-like receptor (TLR) 2 and TLR8 cooperativity and TLR8-mediated induction of IFN-beta. in Proceedings of the National Academy of Sciences of the United States of America 2011
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.
We have thus identified TLR8 as an important driver of follicular helper T cell differentiation
TLR8 is the key RNA-sensing TLR involved in the establishment of fibrosis.
SNPs in TLR8 and TLR9 were associated with the development of tuberculosis; those SNPs may have different effects on disease pathogenesis and progression.
variations in TLR7 and TLR8 genes modulate the clearance and progression of HCV infection with different magnitudes between sexes
Conditioned media or microparticles released from obese omental adipose tissue increased CD16 and CCR5 expression on CD14(+)CD16(-) monocytes and augmented their migratory capacity towards the conditioned media from obese omental adipose tissue, itself.
Btk acts in the TLR7/8 pathway and mediates Ser-536 phosphorylation of p65 RelA and subsequent nuclear entry in primary human macrophages.
Study demonstrates that Hepatitis C virus (HCV) genomic RNA harbours specific sequences that initiate an anti-HCV immune response through TLR7 and TLR8 in various antigen presenting cells.
Thus, TLR7 and TLR8 might modulate different immune responses in monocytes and macrophages.
MBZ-induced IL-1beta release was found to be dependent on NLRP3 inflammasome activation and to involve TLR8 stimulation.
Positive rates of iNOS 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, TLR7, TLR8, NF-kappaB p65, and iNOS in cervical epithelial cells were higher in CC group than in other groups.
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 and TLR8 genetic polymorphisms are associated with susceptibility to mycobacterium tuberculosis infection, and the link is shaped by less effective MTB 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 enhanced localization of HIV-1 with TLR8(+) early endosomes, triggered a pro-inflammatory response, and inhibited trans-infection of CD4(+) 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/TLR8 activation.
This is the first study illustrating certain genotypes of TLR-7 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-like receptors TLR7/8 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 lung tissue explants showed a greater pro-inflammatory response to TLR3 or TLR7/8 activation than control smokers.
The activation of TLR8, TLR7, or TLR3 results in dendritic shortening, and TLR7 and TLR3 but not TLR8 also control axonal growth.
Evaluation of the adjuvant effect of agonists of toll-like receptor 4 and 7/8 in a vaccine against leishmaniasis
TLR8 coupling with SOCS-1 inhibits TLR7-mediated antiviral immunity during WNV infection in mice.
this study shows that beta,beta-dimethylacryloyl alkannin could inhibit psoriasis-activated dendritic cells via the TLR7/8 pathway
mTLR8 is functional and is vital role in the activation of innate immune responses.
an important role of 2'-O-methylation for shaping differential TLR7 or TLR8 activation
Hepatic expression of Tlr6, but not that of Tlr8 is epigenetically controlled, and that the dysregulations of Tlr6 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 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- and TLR7/8-mediated macrophage activation.
These results suggest that IL-23-driven inflammation in mouse skin may be dependent on signaling mediated by TLRs 7, 8, and 9
aortic angiogenesis is preceded by an immune reaction with overexpression of Toll-like receptors (TLRs) and TLR-inducible genes.
Dosage of X-linked Toll-like receptor 8 determines gender differences in the development of systemic lupus erythematosus.
MSCs and MSC-conditioned medium modulate the cytokine expression profile in macrophages following TLR7/8-mediated stimulation, which suggests that MSCs play an immunomodulatory role during ssRNA virus infection
TLR8 controls TLR7 function on dendritic cells, and TLR9 restrains TLR7 response on B cells
A-to-I editing of viral ssRNA directly enhanced mouse Tlr7 and Tlr8 sensing.
our findings indicate a detrimental role for neuronal TLR8 signaling in the triggering of post-stroke inflammation and neuronal death
TLR8 plays an important role in the regulation of TLR7-mediated autoimmunity in the mouse. Review.
Poly-thymidine oligonucleotides act in synergy with TLR7/8 agonists to induce strong TLR7-dependent cytokine production in glial cells.
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.
Knockdown TLR8 increased the apoptosis induced by Bacillus Calmette Guerin infection, and this enhanced apoptosis was caspase-dependent.
A five-amino-acid motif in the undefined region of the TLR8 ectodomain is required for species-specific ligand recognition.
Comparative sequence analysis revealed a total of 139 polymorphisms, which include single-nucleotide polymorphisms and insertion-deletion polymorphisms.
a ligand-induced dimer conformational switch is mainly responsible for TLR8 activation.
multiple regions, including ECD, TM, linker and TIR-tail regions of bTLR8, are involved in determining the localization of cellular ER compartment.
Porcine TLR7 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.