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- Table of Contents
Facts about Toll-like receptor 8.
Acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory reaction. .
Human | |
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Gene Name: | TLR8 |
Uniprot: | Q9NR97 |
Entrez: | 51311 |
Belongs to: |
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Toll-like receptor family |
CD288 antigen; CD288; MGC119599; MGC119600; TLR8; toll-like receptor 8
Mass (kDA):
119.828 kDA
Human | |
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Location: | Xp22.2 |
Sequence: | X; NC_000023.11 (12906620..12923169) |
Detected in brain, heart, lung, liver, placenta, in monocytes, and at lower levels in CD11c+ immature dendritic cells.
Membrane; Single-pass type I membrane protein.
This article will provide information about the TLR8 marker. This article will focus on Steven Boster, High affinity primary antibodies, and TLR8. Learn more about Boster Bio products as well as how to best utilize them in your research. In addition, you'll learn how to use the TLR8 marker in ELISA, Western Blotting, and Immunohistochemistry.
TLR8 detection is difficult to detect using molecular tools. TLR8 studies rely on cell lines that are often not representative of primary human cells. The role of TLR8 is unknown in antibacterial defenses. High-affinity primary antibodies against the TLR8 mark are required to understand the signaling mechanism. TLR8-IRF5 pathway may be a negative regulator.
Using human primary monocytes as models, high-affinity primary antibodies against the TLR-8 marker were found to suppress the production of cytokine-releasing enzymes, which are essential for inflammatory processes. In this study, we used three different concentrations of E. coli (1 x 107/ml), and then exposed the cells to varying levels of the bacteria. We also tested whether TLR8 inhibition inhibited the production of cytokines when human primary monocytes were challenged with different E. coli strains.
TLR8-mediated signaling in human cells inhibits IRAK-1. This receptor is necessary for TLR8-IRF5 signaling, and its activation requires IRAK-1. The nuclear IRF5 levels were measured using IF and scanR analysis. This study showed a significant change in cell activity between cells treated by TLR8 irf-5 activation using TLR8 inhibitors and cells treated with IL-1b, IL-12p70 in a control.
Studies have also shown that BCG vaccinations are associated with protection against hypermorphic TLR8 polymorphism. It has also been linked to protective immunity induced with live attenuated vaccinations. TLR8 is a key factor in TFH cell differentiation, and it is a promising target for vaccine adjuvants. This protein could be used in the future as a biomarker to improve vaccine effectiveness.
Monocytes were transformed into macrophages following transfection using a TLR8 antagonist. The cells were cultured at room temperature in RPMI 1640 containing 10% serum. After transfection, ON-TARGETplus siRNAs were used to stimulate TLR8 signaling. To isolate siRNAs, RNeasy DNAse was used. Maxima cDNA-synthesis kit was used to synthesize the cDNA.
To study the TLR8 response to inflammatory disease, human CD14+CD16-monocytes were used. These cells distinguish between living and dead bacteria and respond with different cytokine profiles. High-affinity primary antibodies against the TLR8 mark are useful for detecting TLR8 Signalling. Here is a list containing high-affinity antibodies against TLR8.
High-affinity primary antibody against the TLR8 marker have shown significant antitumor activities in mice AML and B cells NHL xenograft models. SIRPaIG1 Fc antibodies can cause hemolytic anemia, despite their potential antitumor activities. There are many therapeutic combinations. The SIRPaIG1 Fc antibody is particularly effective in treating cancer by binding with T-cells.
Bispecific T-cell anti CD47 antibodies are effective in blocking expression of T-cell receptors by human T-cells. Bispecific antibodies are also available, such as those that target TLR8-SIRPa. They may be more selective against neoplastics cells and avoid some side effects like monoclonal CD47 antibodies. Further studies will need to consider age of patients before selecting anti-CD47-SIRPa antibodies.
The TLR8 marker is a biomarker to TFH cells. This is a type of macrophage which responds to bacterial RNA. TLR8 activation stimulates TFH cell differentiation and production of IL-21. The bacterial RNA is a potent signal that stimulates TFH cell differentiation. TLR8 is also suppressed by silencing.
Protective immunity is elicited through BCG vaccination in a human cohort when there are high affinity TLR8 variants. This finding implicates TLR8 in TFH cell differentiation. It also suggests that TLR8 could be a target for TFH-skewing vaccine adjuvants. In addition, TLR8 polymorphisms were associated with protective immunity in response to live attenuated vaccines.
Preclinical studies show that RNActive vaccines produce favorable immune responses. These vaccines have been used in the prevention of cancer and other infectious diseases. Researchers found that TLR8 activates immune responses both in mice and in humans. TLR7 in mice is activated by RNActive gene mRNA, while TLR8 activation in humans triggers the production type I and pro-inflammatory substances.
The TLR8 marker is a versatile and useful tool. It is currently being used in clinical studies for many purposes. TLR8 is an integral piece of the immune response, controlling a wide array of inflammatory responses. They include the detection of cytokines, and the identification of tumor-associated cell. These cells secrete IL-12 when stimulated. This cytokine promotes the immune response. However, the results of this study didn't show any significant IL-12 secretion. The authors recommend that the TLR8 marker be used for cancer research.
PMID: 11022119 by Du X., et al. Three novel mammalian Toll-like receptors: gene structure, expression, and evolution.
PMID: 11022120 by Chuang T.-H., et al. Cloning and characterization of a sub-family of human Toll-like receptors: hTLR7, hTLR8 and hTLR9.
*More publications can be found for each product on its corresponding product page