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抗Human TLR9 抗体:
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Dog (Canine) Monoclonal TLR9 Primary Antibody for CyTOF, ELISA - ABIN4360430
Gantner, Hermann, Nakashima, Matsukawa, Sakai, Bacon: CD40-dependent and -independent activation of human tonsil B cells by CpG oligodeoxynucleotides. in European journal of immunology 2003
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Dog (Canine) Monoclonal TLR9 Primary Antibody for FACS, ICC - ABIN4360434
Dillmann, Ringel, Ringleb, Mora, Olesch, Fink, Roberts, Brüne, Weigert: S1PR4 Signaling Attenuates ILT 7 Internalization To Limit IFN-α Production by Human Plasmacytoid Dendritic Cells. in Journal of immunology (Baltimore, Md. : 1950) 2016
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Dog (Canine) Monoclonal TLR9 Primary Antibody for CyTOF, ELISA - ABIN4360432
Damiano, Caputo, Bianco, DArmiento, Leonardi, De Placido, Bianco, Agrawal, Ciardiello, Tortora: Novel toll-like receptor 9 agonist induces epidermal growth factor receptor (EGFR) inhibition and synergistic antitumor activity with EGFR inhibitors. in Clinical cancer research : an official journal of the American Association for Cancer Research 2006
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Dog (Canine) Monoclonal TLR9 Primary Antibody for ELISA - ABIN4360433
Abel, Wang, Fritts, Sanchez, Chung, Fitzgerald-Bocarsly, Krieg, Miller et al.: Deoxycytidyl-deoxyguanosine oligonucleotide classes A, B, and C induce distinct cytokine gene expression patterns in rhesus monkey peripheral blood mononuclear cells and distinct alpha interferon ... in Clinical and diagnostic laboratory immunology 2005
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Human Monoclonal TLR9 Primary Antibody for FACS, IF - ABIN2191964
Ahmad-Nejad, Häcker, Rutz, Bauer, Vabulas, Wagner: Bacterial CpG-DNA and lipopolysaccharides activate Toll-like receptors at distinct cellular compartments. in European journal of immunology 2002
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Human Monoclonal TLR9 Primary Antibody for FACS, IF - ABIN2191962
Rumio, Besusso, Palazzo, Selleri, Sfondrini, Dubini, Ménard, Balsari: Degranulation of paneth cells via toll-like receptor 9. in The American journal of pathology 2004
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Human Monoclonal TLR9 Primary Antibody for FACS, IF - ABIN2191963
Rutz, Metzger, Gellert, Luppa, Lipford, Wagner, Bauer: Toll-like receptor 9 binds single-stranded CpG-DNA in a sequence- and pH-dependent manner. in European journal of immunology 2004
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Human Monoclonal TLR9 Primary Antibody for FACS, IHC (fro) - ABIN531988
Wong, Cheung, Ip, Lam: Intracellular signaling mechanisms regulating toll-like receptor-mediated activation of eosinophils. in American journal of respiratory cell and molecular biology 2007
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Mouse (Murine) Polyclonal TLR9 Primary Antibody for IHC - ABIN967190
Hemmi, Takeuchi, Kawai, Kaisho, Sato, Sanjo, Matsumoto, Hoshino, Wagner, Takeda, Akira: A Toll-like receptor recognizes bacterial DNA. in Nature 2000
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Dog (Canine) Monoclonal TLR9 Primary Antibody for ELISA, FACS - ABIN4360452
Tengroth, Arebro, Kumlien Geor��n, Winqvist, Cardell: Deprived TLR9 expression in apparently healthy nasal mucosa might trigger polyp-growth in chronic rhinosinusitis patients. in PLoS ONE 2014
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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.
infection with dengue virus (DENV), an RNA virus, activates TLR9 in human dendritic cells (DCs).
Intracellular IFN-gamma production upon stimulation with TLR2 and TLR9 ligands.
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
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
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.
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.
the polymorphisms in TLR7 and TLR9 are associated with asthma-related phenotypes and asthma risk in the study population.
Results show that cell-free DNA (cfDNA) could promote colorectal cancer cell proliferation via Toll-like receptor 9 (TLR9) and induced robust release of chemokine interleukin 8 (IL-8; CXCL8 Chemokine).
Study finding indicated that TLR9 may serve as a serological marker for nonsmall cell lung cancer identification.
in patients with chronic forms of Epstein-Barr virus infection, analysis of the T/C polymorphism of the TLR-9 gene revealed three main genotypes - TT, TC, CC; investigation of the frequency of occurrence of individual genotypes revealed the dominance of genotype TC, compared with the homozygous genotypes of TT and CC
There is a relationship between sepsis-induced immunosuppression and serum TLR-9 levels. The host immunity system can be activated by means of TLR-9-related systems, while hyperlactatemia may play a stimulating role in the re-activation of the immune system.
TLR9 is capable of robustly suppressing angiogenesis by differentially regulating the expression of VEGFA and sFLT1 at the fetomaternal interface, potentially contributing to the development of Preeclampsia.
rs187084 AA genotype of TLR9 is associated with Hepatitis B virus progression to advanced liver disease
SNPs in TLR8 and TLR9 were associated with the development of tuberculosis; those SNPs may have different effects on disease pathogenesis and progression.
This study provides evidence that TLR9 affects human S. aureus immunity and present potential explanations for differences according to sex in S. aureus colonization and infection.
decrease in full-length protein levels in substantia nigra of Parkinson disease patients
The authors showed that dendritic cell treatment with a TLR9 agonist results in an increase in fungicidal activity of these cells against the fungus Paracoccidioides brasiliensis.
TLR9 activation is augmented by short single-stranded DNA degradation products
The detection of higher frequencies of the TLR2, TLR4 and/or TLR9 polymorphisms in colorectal cancer (CRC) patients compared with the control groups highlight the role of these polymorphism in CRC development and cancer progression
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.
Contact hypersensitivity immune response was markedly increased in TLR2-deficient or TLR9-deficient NOD mice.
These results suggest that TLR9 contributes to C57BL/6 mouse resistance against L. amazonensis, and that the TLR9-binding LaAg comprising CpG motifs may be important for intranasal vaccine efficacy against cutaneous leishmaniasis .
High TLR9 expression causes inflammatory myopathy.
These data indicate that sepsis-induced cardiac dysfunction requires presence of TLR3 and TLR9 and may be linked to histone-induced damage of cardiomyocytes.
resulting in maturation-specific stabilization of TLR9 within endolysosomes and subsequent pro-inflammatory signaling
data thus indicates that EBV DNA itself acts as a modulator of the Th17 compartment as well as that of regulatory T cell mechanisms. The involvement of TLR9 in the EBV DNA-triggered induction of IL-17A.
Microglial glucocorticoid receptors regulate TLR9 trafficking and lysosomal environment. Loss of glucocorticoid receptors enables activation of a microglial TLR9 inflammatory pathway, which can play a role in the progression of Parksinson disease.
Study shows that placental and/or fetal DNA stimulates toll-like receptor 9 (TLR9) leading to secretion of pro-inflammatory cytokines by macrophage cells.
Plasmodium DNA induces autoreactive responses against erythrocytes by activating a population of B cells expressing CD11c and the transcription factor T-bet, which become major producers of autoantibodies that promote malarial anaemia.
Our findings suggested the collaboration of TLR2-TLR9 at least in the regulation of SARM expression.
High cholesterol intake exacerbated acetaminophen-induced acute liver injury via the accumulation of free cholesterol in the endolysosomes of liver sinusoidal endothelial cells. This accumulation enhanced Toll-like receptor 9 signaling via impairment of its membrane trafficking mechanism.
these data provide a previously uncharacterized in vivo mechanism contingent on oligodeoxy-nucleotide -administered dose, where TLR9 governs the primary response and RAGE plays a distinct and cooperative function in providing a pivotal role in balancing the immune response.
this study shows that CD205-TLR9-IL-12 axis contributes to CpG-induced oversensitive liver injury in Hepatitis B viral antigens transgenic mice by promoting the interaction of NKT cells with Kupffer cells
The findings support a salutary role of TLR9 in some subsets of HF conditions and underline the importance for future studies on the mechanisms of TLR9 in diastolic HF.
TLR9-driven inflammation induced a Ccr2-independent expansion of functionally enhanced extramedullary myeloid progenitors that correlated with the peripheral accumulation of monocytes in both wild-type and Ccr2(-/-) mice.
TLR9 expression on B1a cells is not critical for their IgM-dependent atheroprotection.
This study establishes a correlation between TLR-3 and TLR-9 expression with the development of EAE. In addition, evidence of a role for the myelin peptide in targeting the innate inflammatory response to the CNS is presented.
these results indicate clear responses of porcine neonatal antigen presenting cells after TLR2 and TLR9 stimulation
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.
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.
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.
expression of TLR3, TLR7 and TLR9 in alveolar macrophages infected with different genotype 1 PRRSV strains
we studied TLR9 expression in lung extracts from pigs, dogs, and cattle.
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.
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
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
substantial conservation of TLR9 structure and TLR9 function in blood leukocytes
Comparative sequence analysis revealed a total of 139 polymorphisms, which include single-nucleotide polymorphisms and insertion-deletion polymorphisms.
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 preferentially expressed in immune cell rich tissues, such as spleen, lymph node, bone marrow and peripheral blood leukocytes. Studies in mice and human indicate that this receptor mediates cellular response to unmethylated CpG dinucleotides in bacterial DNA to mount an innate immune response.
Toll-like receptor 9 protein