Aperçu des produits pour TLR9 Protéines (TLR9)

Human Toll-Like Receptor 9 (TLR9) interaction partners

1. TLR9-1237T/C gene polymorphism may not be considered as a molecular risk for patients with Hepatitis C in Pakistan.

2. present study results demonstrate no involvement of TLR9 C296T/ Pro99Leu polymorphism in cervical cancer susceptibility and supports worldwide minor allele frequency (MAF) (0.0002) status of the same as no nucleotide variation was detected in any of the study participants

3. Modulation of TLR9 signaling pathways and decrease of macrophage-mediated inflammation might be potential therapeutic strategies in LMNA-RM management.

4. This study characterizes a strategy to apply localized TLR9 stimulation to a tumor type not accessible for direct injection, a strategy that may expand the therapeutic potential of PD-1 blockade in non-small cell lung cancer

5. Protein concentration of TLR-9 was significantly higher in tumors of gastro-esophageal junction cancer with lymph node metastasis and depth of tumor invasion.

6. TLR9 binding site exhibits a strong bias in favor of a phosphodiester backbone over the phosphorothioate backbone of the CpG motif. Furthermore, while single point mutations of W47, W96 and K690 within the TLR9 binding site retains full TLR9 activation by phosphodiester-based oligodeoxynucleotides, activation by phosphorothioate-based oligodeoxynucleotides is strongly impaired.

7. TLR9 expression and function were significantly suppressed in a cohort of chronic hepatitis B virus carriers

8. Mitochondrial DNA contains CpG motifs that incite proinflammatory signaling through the endosomal, nucleotide-sensing Toll-like receptor, TLR9.

9. Our results demonstrate a defect of the TLR9 responses in IgA deficiency that leads to B cell dysregulation and decreased IgA production.

10. 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.

11. these results show a direct engagement of TLR9 ligand in T helper cells

12. TLR9 polymorphisms were screened in 131 chronic hepatitis B patient and 168 individuals by polymerase chain reaction (PCR) - restriction fragment length polymorphism (RFLP) technique

13. 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.

14. infection with dengue virus (DENV), an RNA virus, activates TLR9 in human dendritic cells (DCs).

15. Intracellular IFN-gamma production upon stimulation with TLR2 and TLR9 ligands.

16. The ability to form complexes with DNA and to subsequently activate TLR9 is thought to be related to the cationicity of the peptides and to secondary structure, because a predominant alpha-helical structure was shown to stabilize the peptide-DNA interaction

17. TLR9 signaling might enhance antibody titers at the expense of the ability of B cells to engage in germinal-center events that are highly dependent on B cells' capture and presentation of antigen

18. TLR9 1635AA genotype is associated with lower CD4 counts in HIV positive patients.TLR9 1635AA polymorphism correlates with higher plasma IP10 levels in HIV infected patients.

19. the authors provide an overview on the contribution of TLR7 and TLR9 to autoimmune diseases and discuss recent findings indicating a pivotal role for these two receptors, along with Epstein-Barr virus, in driving, perpetuating, and/or amplifying intrathymic B cell dysregulation and autoimmune responses in myasthenia gravis.

20. the polymorphisms in TLR7 and TLR9 are associated with asthma-related phenotypes and asthma risk in the study population.

Mouse (Murine) Toll-Like Receptor 9 (TLR9) interaction partners

1. TLR-9-driven signals potentiate the effects of IFNgamma to initiate murine macrophage activation syndrome (MAS), and induction of inflammatory myelopoiesis is a common TLR-9- and IFNgamma-dependent pathway that may contribute to the pathogenesis of MAS.

2. TLR9 is involved in the pathogenesis of erosive autoimmune arthritis.

3. Study used Yaa mice as a model of autoimmune membranoproliferative glomerulonephritis (MPGN) to show that overexpression of Tlr9 and its downstream factors in the glomerulus correlated with podocyte injury and progression of autoimmune MPGN.

4. A toll-like receptor 9 antagonist restores below-level glial glutamate transporter expression in the dorsal horn following spinal cord injury.

5. Data show that toll-like receptor 9 (TLR9) signaling by CpG, while promoting vigorous proliferation, completely fails to induce differentiation of toll-like receptor 9 (FO B) cells into plasmablasts and plasma cells (PBs/PCs).

6. A critical role of CD180 in regulating TLR7- and TLR9-mediated activation of macrophages and DCs.

7. model of systemic autoimmunity that depends on T cell detection of a membrane-bound OVA fusion protein expressed by MHC class II+ cells, expression of TLR7, expression of the type I IFN receptor, and loss of expression of TLR9, with a high frequency of OVA-specific Tbet+, IFN-gamma+, and FasL-expressing Th1 cells as well as autoantibody-producing B cells

8. This study characterizes a strategy to apply localized TLR9 stimulation to a tumor type not accessible for direct injection, a strategy that may expand the therapeutic potential of PD-1 blockade in non-small cell lung cancer

9. Data suggest a direct link between microtubule-associated protein 1-light chain 3 (LC3)-associated phagocytosis (LAP) formation and IKK alpha (IKKalpha) recruitment downstream of -like receptor 9 (TLR9) activation that is necessary to facilitate type I IFN production.

10. data extend previous studies, demonstrating that rfd phages induce Ag-specific IgG and CD8(+) T cell-mediated responses and confer protection against an important human parasite infection, through a TLR9-dependent mechanism.

11. TLR9 binding site exhibits a strong bias in favor of a phosphodiester backbone over the phosphorothioate backbone of the CpG motif. Furthermore, while single point mutations of W47, W96 and K690 within the TLR9 binding site retains full TLR9 activation by phosphodiester-based oligodeoxynucleotides, activation by phosphorothioate-based oligodeoxynucleotides is strongly impaired.

12. TLR7 and TLR9 specify monocyte fate and identify a specialized population of phagocytes responsible for anemia and thrombocytopenia associated with inflammation and infection.

13. this study shows that TLR9 promotes mobilization of pulmonary dendritic cells during beryllium sensitization

14. Mitochondrial DNA contains CpG motifs that incite proinflammatory signaling through the endosomal, nucleotide-sensing Toll-like receptor, TLR9.

15. dual TLR2/9 recognition plays a critical role in providing resistance against mucosal infection with HSV

16. Mitochondrial DNA activates neutrophils via cyclic GMP-AMP synthase (cGAS)-STING and the Toll-like receptor 9 (TLR9) pathways and increases the production of neutrophil elastase and extracellular neutrophil-derived DNA in neutrophil extracellular traps.

17. TLR9 signaling in other cell types may promote cytoprotective effects.

18. TLR9-specific CPDP that targets both receptor dimerization and adapter recruitment.

19. Although most TLR9-CpG DNA interactions are conserved among species, some are unique to mice and involved in species-specificity. These findings provide the structural basis for how mouse TLR9 dimerizes efficiently in response to CpG DNA to activate innate immunity.

20. on repeated toll-like receptor 9 (TLR9) stimulation with unmethylated cytosine guanine dinucleotide containing single-stranded DNA (CpG), IL-18BP(-/-) mice display severe MAS manifestations, including increased weight loss, splenomegaly, anemia, thrombocytopenia, hyperferritinemia, and bone marrow hemophagocytosis as compared with wild-type mice.

Pig (Porcine) Toll-Like Receptor 9 (TLR9) interaction partners

1. endotracheal tube presence was characterized by neutrophil activation, necrosis, and release of proinflammatory cytokines mediated by TLR9/NF-kappaB induction.

2. these results indicate clear responses of porcine neonatal antigen presenting cells after TLR2 and TLR9 stimulation

3. Porcine parvovirus virus infection significantly induced IL-6 expression and this induction depended on NF-kappaB activation and TLR9 signaling pathways in PK-15 cell.

4. TLR9 immunoreactivity is mainly detected in epithelial cells and antigen presenting cells, namely dendritic and macrophage-like cells, within the range of tissues examined. The pattern of TLR9 expression was similar in pigs of 3 weeks and 3 months of age.

5. 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.

6. expression of TLR3, TLR7 and TLR9 in alveolar macrophages infected with different genotype 1 PRRSV strains

7. we studied TLR9 expression in lung extracts from pigs, dogs, and cattle.

8. Moreover, the TLR9 transfectant demonstrated its usefulness for evaluation of immunostimulation by bacterial DNA through the detection of T(H)-1, T(H)-2 type cytokine induction via TLR9 signaling.

Cow (Bovine) Toll-Like Receptor 9 (TLR9) interaction partners

1. variants in the TLR1 gene are associated with susceptibility to bovine tuberculosis, whereas no significant association can be inferred from the polymorphisms in the TLR9 gene

2. we studied TLR9 expression in lung extracts from pigs, dogs, and cattle.

3. mRNA abundances of TLR9, TLR2, and TLR4 together with those of beta-defensin 5 (BNBD5), an early bactericidal effector molecule of the innate system, in healthy and infected mammary glands

4. substantial conservation of TLR9 structure and TLR9 function in blood leukocytes

5. Comparative sequence analysis revealed a total of 139 polymorphisms, which include single-nucleotide polymorphisms and insertion-deletion polymorphisms.