Ask about this productRelated genes to: TLR8 antibody
- 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 antibody
Related articles to: TLR8 antibody
- We report a case of a 25-year-old male with recurrent oral ulcers, upper respiratory tract infections, and an 8-year history of chronic neutropenia. Previously diagnosed with Behçet's disease, the patient had undergone comprehensive hematological evaluations at multiple tertiary institutions, yet the etiology of his persistent neutropenia remained undetermined. Whole-exome sequencing revealed a -G572D mutation, leading to a diagnosis of autoimmune myelofibrosis (AIMF) secondary to gain-of-function (GOF). While concurrent Behçet's disease and neutropenia may occur clinically, the underlying pathogenesis is often neglected. -GOF screening should be emphasized in young patients with such presentations. To our knowledge, this is the first reported association between -GOF mutation and AIMF, expanding the phenotypic spectrum of TLR8-related disorders. - Source: PubMed
Publication date: 2026/04/12
Qu ShiqiangZhang PeihongXu ZefengQin TiejunLi BingXiao Zhijian - Multiple heterocyclic scaffolds have been found to exhibit agonist or antagonist activity at toll-like receptors (TLRs) with varying degrees of selectivity for the subtypes. TLR7 and 8 agonists are potentially valuable vaccine adjuvants while antagonists show useful activity against autoimmune diseases and cancer. A pyrazolo[1,5-c]quinazoline based compound 23, an unexplored scaffold in the domain of TLR7/8, was synthesized by analogy with lead agonists and antagonists from the literature. Compound 23 exhibited moderate agonist activity for both TLR7 and TLR8. The effect of structural modifications at the C1, C8, C9, and C10 position of the pyrazolo[1,5-c]quinazoline scaffold on hTLR7/8 activity was investigated by synthesizing a focused library of compounds. Although none of the compounds had agonist activity, three compounds were found to be dual TLR7/8 antagonists. These findings add to the existing structure-activity relationship knowledge of the tricyclic TLR7/8 modulators that will aid subsequent discovery and optimization of new drug candidates. - Source: PubMed
Kumar KushvinderHonda-Okubo YoshikazuDas Pradeep KDixit AnshumanSingh Kamal NainWinkler David APetrovsky NikolaiSalunke Deepak B - Antibody-dependent enhancement (ADE) of dengue virus-type 2 (DENV2) is a major risk factor for severe disease, facilitating Fcγ receptor-mediated viral entry and triggering inflammation that compromises vascular integrity. While Toll-like receptor 2 (TLR2) on monocytes promotes DENV2, strain 16681 infection in these cells and triggers an inflammatory response that activates the endothelium, its contribution to ADE remains unclear. Here, using peripheral blood mononuclear cells, we compared FcγRII (CD32)-mediated ADE infection with direct infection and assessed the contributions of TLR2, RNA sensors (TLR8, TLR3), and spleen tyrosine kinase (SYK). Blocking CD32 or SYK reduced antibody-enhanced infection to direct infection levels, whereas TLR2 inhibition abolished infection entirely. Furthermore, TLR8, TLR3, and SYK mediated inflammatory responses under both ADE and direct infection. These findings identify TLR2 as indispensable also for CD32/SYK-driven viral entry and implicate TLR8, TLR3, and SYK in ADE-associated inflammation. Our study provides mechanistic insight into ADE pathogenesis and highlights potential targets for mitigating severe dengue outcomes. - Source: PubMed
Publication date: 2026/04/17
Ter Ellen B MPunekar MCastillo J AValdés-López J FUpasani VSann SKarnthaler MMartija BMoser JSmit J MCantaert TRodenhuis-Zybert I A - Sepsis remains a leading cause of morbidity and mortality worldwide, with outcomes highly influenced by host immune responses. While environmental and pathogen-related factors are well recognized, the contribution of host genomic variants to sepsis susceptibility and severity is increasingly appreciated. Because approximately 85% of known disease-causing mutations reside in the exome, whole exome sequencing (WES) offers a powerful strategy to uncover pathogenic variants in critically ill patients and to identify potential inborn errors of immunity that may modulate disease course. In the present study, we performed WES on 31 sepsis patients across different age groups, stratified into pre-school-aged children, school-aged children, and adults, and identified multiple genes harboring high- or medium-impact variants. Of particular interest, a high-impact TLR8 variant (rs3764880: A>G; p.Met1Val) was observed across all the age groups and predominantly in individuals with bacterial sepsis. Single-cell RNA sequencing of peripheral blood mononuclear cells demonstrated that TLR8 was highly expressed in non-classical monocytes, with transcription levels markedly elevated in carriers of the variant. Functional studies revealed that this TLR8 variant enhanced IFN-β secretion upon ligand stimulation, suggesting that dysregulated TLR8 signaling might modulate host inflammatory responses during bacterial sepsis. Given the established role of IFN-β in exacerbating sepsis severity, these findings support a model in which the TLR8 rs3764880 variant contributes to sepsis pathophysiology by amplifying IFN-β-mediated monocyte responses. This study underscores the importance of integrating genomic and functional immunologic analyses to identify host determinants of sepsis, highlights TLR8 as a potential biomarker and therapeutic target, and provides a framework for precision medicine approaches to predict and modulate outcomes in bacterial sepsis. - Source: PubMed
Publication date: 2026/04/15
Alhamdan FahdGianoli StefanoHan XioahuiKoutsogiannaki Sophia - Newborns are particularly vulnerable to nosocomial infection, but the underlying mechanisms are incompletely understood. Age-dependent differences in the expression of innate immune receptors and thus a reduced or delayed antimicrobial host response might contribute. Here we discovered that neonatal cord blood monocytes (CBMo) express lower levels of Toll-like receptor TLR8 but similar levels of TLR7 as compared to adult peripheral blood monocytes (PBMo). We investigated the TLR7/8 signal transduction by stimulating monocytes of adults (PBMo) and neonates (CBMo) with imiquimod (R) and resiquimod (R). Toll-like receptors (TLRs) bind various constituents of invading pathogens and trigger defense reactions. We found differential expressions of TLR7 and TLR8 which both bind to ssRNAs. We could show, that inflammatory cytokine response represented by TNF-α is comparable in PBMo and CBMo. This effect was stronger in resiiquimod (R) treated PBMo and CBMo. Whereas IL-6 secretion was found similar induced in PBMo and CBMo after stimulation with TLR7/8 ligands, IL-10 was only induced in PBMo, biasing the cytokine answer to the pro-inflammatory response in CBMo. Cytokine response was more dependent to NFκB signaling although MAP kinase activation was required for the IL-6 response in CBMo. The type 1 interferon response was found comparable in PBMo and CBMo and was correlated to IRF-7 activation. We utilized an in vitro model of gram-negative bacterial (E. coli) infection to study whether TLR7/8 pre-stimulation influence peri-phagocytic reactions. TLR7/8 pre-stimulation modified the E. coli PAMP receptor CD14 and CD32 expression. IL-6 and IL-10 secretion was not altered by TLR7/8 stimulation prior to infection. TLR7 pre-stimulation reduced E. coli survival in CBMo, but was not accompanied by higher TNF-α levels. Administration of imiquimod (R) displays therefore beneficial aspects for opportunistic bacterial infections in-vitro. - Source: PubMed
Publication date: 2026/04/13
Dreschers SHeiler EOppermann LGille CHornef MOrlikowsky T W