TLR8 pAb
- Known as:
- TLR8 pAb
- Catalog number:
- ASA905711100
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- TLR8 pAb
Related genes to: TLR8 pAb
- Gene:
- TLR8 NIH gene
- Name:
- toll like receptor 8
- Previous symbol:
- -
- Synonyms:
- CD288
- Chromosome:
- Xp22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-27
- Date modifiied:
- 2016-10-05
Related products to: TLR8 pAb
Related articles to: TLR8 pAb
- Bepirovirsen is an unconjugated antisense oligonucleotide in Phase 3 trials for chronic hepatitis B virus (HBV) infection. Post hoc analyses from a Phase 2a study (chronic HBV participants) indicated immediate cytokine production upon dosing of bepirovirsen, leading to the hypothesis that bepirovirsen may have innate immune stimulatory activity via pattern recognition receptors (PRRs) in hepatic non-parenchymal cells, alongside its known direct antiviral mechanism in hepatocytes. - Source: PubMed
Publication date: 2026/06/09
Ermler Megan EDelahaye Jared LJordan WilliamNivarthi UshaDeHart AnneJones KristenDas AmitabhGalwey NicholasHoang BaoTerry Rebecca LTarrant JimmySherina ValeriiaRay AvijitAustin DarenSingh Jennifer MTheodore DickensPaff MelanieYou Shihyun - Toll-like receptor 8 (TLR8) is crucial for detecting viral and bacterial ssRNA in mammals. However, its functional characteristics in early vertebrates remain largely unclear. Here, we employed the economically important fish Ctenopharyngodon idella, which harbors two TLR8 homologs (CiTLR8a/b), as a representative model. CiTLR8a/b are trafficked to early endosomes and lysosomes by UNC93B1, where they dynamically form homodimers and heterodimer, and bind ssRNA and dsRNA. Upon ligand binding, they first recruit MyD88, then TIRAP as adaptors. Unexpectedly, CiTLR8a enhances viral replication by suppressing downstream IFN, NF-κB, and AP-1 pathways in vitro and in vivo. In contrast, CiTLR8b is signaling-defective despite ligand binding and adaptor recruitment. Most strikingly, heterodimerization with signaling-inert CiTLR8b switches CiTLR8a into an antiviral sensor by remodeling intracellular TIR-domain conformation through extracellular LRR-ligand interaction. Further, structural and mutagenesis analyses identify critical functional determinants: specific residues (CiTLR8a-V116/S164; CiTLR8b-S43/N790) required for dsRNA binding, and key N-glycosylation sites (N138/N189) and cysteines (C3/C4/C6/C7) in CiTLR8a responsible for its proviral functions, with Cys6/Cys7 being critical for CiTLR8a/b proper localization. TLR8 evolution follows a stepwise pattern: absent in cyclostomes, it emerges in jawed vertebrates and expands via lineage-specific duplications (whole-genome in teleosts; tandem in amphibians/reptiles), is lost in avians, and persists as a single copy in mammals. Notably, Cyprinid TLR8 can bind dsRNA besides ssRNA. Collectively, our findings elucidate the functions, adaptive mechanisms, and evolutionary trajectory of TLR8 in lower vertebrates, uncovering a unique regulatory system involving its two homologs. These results offer a new perspective on how TLR evolution shapes vertebrate immune system. - Source: PubMed
Publication date: 2026/06/04
Zhang JingjingLv MaolinWang ShijieXu YuezongWang PengxuTang BoLiao ZhiweiJiang RuiChen GuanyuXiong NingxiaYang ChunrongLiu JingxiaSu Jianguo - Polyvalent IgG (pIgG/IVIg), derived from thousands of donors, exerts broad immunomodulatory effects; however, its direct cellular targets and genome-wide regulatory impacts remain incompletely defined. - Source: PubMed
Publication date: 2026/05/30
Borges João Vitor da SilvaPassos Lhays OzórioMachado Nicolle Rakanidisdo Nascimento Lais AlvesFagundes Beatriz OliveiraBergamasco Isabela SiuffiMoreira Anna Luisa BaratelliCilento Natali EspasianiSanabani Sabri SaeedVictor Jefferson Russo - The diagnosis of pulpal inflammatory conditions poses significant challenges in clinical endodontics, requiring precise differentiation between reversible and irreversible states. This study investigated the differential expression patterns of 10 inflammatory genes: LCP2, PTPRC, CXCL8, TNFα, IL6, CCL2, MMP9, NOD2, ICAM1, and TLR8 in irreversible pulpitis as potential molecular diagnostic biomarkers. - Source: PubMed
Publication date: 2026/05/30
Bhat RakshaD'souza Sean PrinsonShetty PreetheshPadavu ShruthiRai PraveenKrishna Kumar BallamooleShetty Shishir - To investigate the ameliorative effect of menstrual blood-derived mesenchymal stem cells (MenSCs) on liver fibrosis and injury, and further study whether it plays a role by regulating the Toll-like receptor (TLR) signaling pathway in a mouse model of alcoholic liver disease (ALD). A C57BL/6J mouse model of ALD was established using the gradient ethanol gavage method combined with pyrazole. A blank control group and a model group were established. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (GGT) activities, as well as inflammatory factors, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), were measured. The modeling effect was evaluated by combining Masson staining and Sirius red staining in liver tissue with Western blotting to detect the protein expression of α-smooth muscle actin (α-SMA) and collagen type I α1 chain (COL1A1). Simultaneously, qPCR was used to detect the mRNA expression of TLRs and transforming growth factor β-activated kinase 1 (TAK1) to explore the related mechanisms. ALD model mice were divided into a phosphate-buffered saline (PBS) control group and a MenSCs treatment group [2×10⁵ MenSCs (200 μL) injected via tail vein], with intervention once a week sustained for four weeks after successful modeling. Mice batches were sacrificed on the seventh day following each intervention to collect serum and liver tissues. Collagen deposition changes were observed using Sirius red staining. The expression of α-SMA and transforming growth factor-β1 (TGF-β1) proteins was detected by Western blotting. Serum biochemical indicators levels were also measured. The effects of MenSCs on TLRs and TAK1 mRNA expression were assessed using qPCR to comprehensively evaluate the MenSCs intervention effect. The two groups were compared using paired -tests. Repeated measures analysis of variance (RM-ANOVA) combined with Tukey's multiple comparisons test was used for comparisons among multiple groups. Compared with the blank control group, serum levels of ALT, AST, and GGT, as well as inflammatory factors TNF-α and IL-6, were significantly elevated, while IL-1β levels were significantly decreased in the mouse model of the ALD group. Collagen deposition in liver tissue was markedly increased. The expression of fibrosis markers α-SMA and COL1A1 proteins was significantly upregulated (α-SMA: <0.001; COL1A1: <0.001). The mRNA expression of TLR1, TLR2, TLR4, TLR6, TLR7, and TLR8 was significantly upregulated, and the expression of TLR9 and TAK1 was downregulated, while the expression of TLR3 and TLR5 remained unchanged. Liver function levels (ALT and AST) were significantly reduced; liver fibrosis degree was markedly improved; and TGF-β1 and α-SMA protein expression were suppressed (TGF-β1: <0.001; α-SMA: =0.026) following MenSC transplantation in mice. MenSC specifically down-regulated the mRNA expression of TLR1, TLR2, TLR4, TLR6, TLR7, and TLR9, with significant inhibition of TLR1, TLR2, and TLR9 expression (<0.001), while TLR8 and TAK1 expression were not significantly affected at week 4 of intervention (>0.05). MenSCs transplantation can effectively improve liver function and reduce fibrosis in a mouse model of ALD, and its mechanism may be related to the inhibition of the TLR signaling pathway activation. - Source: PubMed
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