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  • mProX™ Human TLR8 Stable Cell Line

    [CAT#: S01YF-1023-PY214]
    Product Category:
    Membrane Protein Stable Cell Lines
    Subcategory:
    Immune Checkpoint Cell Lines

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    Product Information

    Target Family
    Immune Checkpoint
    Target Protein Species
    Human
    Host Cell Type
    HEK293;CHO-K1;HL-60;OCI-AML-3
    Target Classification
    Immune Checkpoint Cell Lines
    Target Research Area
    Immunology Research
    Related Diseases
    Immunodeficiency 98 With Autoinflammation, X-Linked; Anemia, Autoimmune Hemolytic
    Gene ID
    Human:51311
    UniProt ID
    Human:Q9NR97

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    Toll-like receptor 8 (TLR8) shares similarities with TLR7 in recognizing single-stranded RNA. However, its specific role and significance in the immune system have distinct nuances. Recent studies have shown that TLR8 plays a role in recognizing viral infections, including SARS-CoV-2 and HIV-1. Moreover, TLR8 mutations have been associated with autoimmune and autoinflammatory disorders, suggesting its intricate role in immune regulation. Given its importance in recognizing viral pathogens, TLR8 is being explored as a potential therapeutic target in antiviral strategies.

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    FAQ

    chat Taylor Davis (Verified Customer)

    How does simvastatin affect TLR8 signaling? May 22 2020

    chat Patrick Liam (Creative Biolabs Scientific Support)

    Simvastatin inhibits TLR8 signaling in human monocytes, which may partly explain its anti-inflammatory effects. This mechanism of action of simvastatin on TLR8 signaling is previously unrecognized. May 22 2020

    chat Skyler Williams (Verified Customer)

    What is the role of UNC93B1 in TLR8-mediated signaling? Nov 09 2021

    chat Patrick Liam (Creative Biolabs Scientific Support)

    UNC93B1 is crucial for TLR8 localization to the early endosome and the ER, regulating TLR8-mediated signaling in human monocytes. This finding indicates a differential regulation of TLR localization for each TLR. Nov 09 2021

    Published Data

    Fig.1 TLR8 overexpression boosts the R848-induced rise in the CD11b lineage marker.

    TLR8 overexpression boosts the R848-induced rise in the CD11b lineage marker. TLR8-mCherry plasmid transfected HL60 and OCI-AML3 cells were treated with R848. Cells were stained for CD11b and gated based on the presence or lack of mCherry after at least 72 hours. TLR8 activation resulted in statistically significant variations in CD11b expression in untreated HL60, treated HL60, and OCI-AML3 cells. * denotes P<0.05, ** denotes P<0.01.

    Ref: Ignatz-Hoover, James J., et al. "The role of TLR8 signaling in acute myeloid leukemia differentiation." Leukemia 29.4 (2015): 918-926.

    Pubmed: 25283842

    DOI: 10.1038/leu.2014.293

    Research Highlights

    Yeong Ha, Jae. et al. "Periodontitis promotes bacterial extracellular vesicle-induced neuroinflammation in the brain and trigeminal ganglion." PLoS pathogens, 2023.
    Extracellular vesicles (EVs) released by Gram-negative bacteria, specifically the periodontopathogen Aggregatibacter actinomycetemcomitans (Aa), have been studied extensively for their role in various inflammatory diseases. Recent research has revealed that these EVs are capable of crossing the blood-brain barrier and inducing the secretion of proinflammatory cytokines in the brain through their RNA cargo. In order to further investigate the connection between periodontal disease (PD) and neuroinflammatory conditions, a mouse model of ligature-induced PD was utilized. Upon administration of Aa EVs through intragingival injection or EV-soaked gel, strong induction of cytokines was observed in the brains of PD mice. TLR (Toll-like receptor)-reporter cell lines and MyD88 knockout mice were utilized to confirm that the release of cytokines was stimulated by Aa EVs via the TLR4 and TLR8 signaling pathways and their downstream MyD88 pathway. Additionally, it was discovered that the injection of EVs through the skin and gingival tissues resulted in the retrograde transfer of Aa EVs, from axon terminals to the cell bodies of trigeminal ganglion (TG) neurons, subsequently activating these neurons. Moreover, the action potential of TG neurons was also shown to be affected by Aa EVs. These findings suggest that EVs derived from periodontopathogens such as Aa may play a role in the development of neuroinflammatory diseases, neuropathic pain, and other systemic inflammatory symptoms as a comorbidity of periodontitis.
    Yeong Ha, Jae. et al. "Periodontitis promotes bacterial extracellular vesicle-induced neuroinflammation in the brain and trigeminal ganglion." PLoS pathogens, 2023.
    Pubmed: 37871107   DOI: 10.1371/journal.ppat.1011743

    G DeYoung, Emma. et al. "Synthesis and Optimization of 1-Substituted Imidazo [4, 5-c] quinoline TLR7 Agonists." ACS medicinal chemistry letters, 2023.
    Recently, a highly potent TLR7 selective agonist has been reported to have significant therapeutic potential in various oncology and autoimmune applications. TLR7 agonists have drawn attention as a potential treatment due to their ability to activate the immune system and elicit anti-tumor and anti-inflammatory responses. This promising agent may prove to be a valuable addition to the existing arsenal of treatments for these conditions.
    G DeYoung, Emma. et al. "Synthesis and Optimization of 1-Substituted Imidazo [4, 5-c] quinoline TLR7 Agonists." ACS medicinal chemistry letters, 2023.
    Pubmed: 37849530   DOI: 10.1021/acsmedchemlett.3c00260

    Please note: All products are "FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC OR CLINICAL PROCEDURES" For licensing inquiries, please contact
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