mProX™ Human TLR8 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Immune Checkpoint Cell Lines
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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