Polyclonal TLR8 (IN)
- Known as:
- Polyclonal TLR8 (IN)
- Catalog number:
- pc-447
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal TLR8 ()
Related genes to: Polyclonal TLR8 (IN)
- 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: Polyclonal TLR8 (IN)
Related articles to: Polyclonal TLR8 (IN)
- Systemic lupus erythematosus (SLE) is a disease with considerable unmet treatment needs. Endosomal nucleic acid sensing by Toll-like receptor 7 (TLR7) is emerging as a key pathogenic pathway. Gain-of-function mutations in the genes encoding TLR7 and its chaperone UNC93B1 can cause monogenic childhood-onset SLE; rare variants in proteins that regulate ligand availability or downstream signalling proteins also contribute to disease. TLR7 variants can increase the affinity of this receptor for its ligands and can alter binding to endogenous antagonists. Both self RNA-protein complexes and viruses have been implicated in TLR7 activation. Key pathogenic mechanisms include breakdown in B cell tolerance and autoantibody production and type I interferon secretion. Although current therapies such as B cell-depleting chimeric antigen receptor (CAR) T cells and anifrolumab (anti-type I interferon receptor) offer benefit, they are limited by high costs and lack of oral options. In this context, TLR7 has emerged as a promising therapeutic target. Phase II trials of an oral dual TLR7-TLR8 antagonist show durable suppression of the interferon signature in all patients, indicating that TLR7 and TLR8 drive this signature in SLE. This treatment has shown clinical benefit for SLE and cutaneous lupus erythematosus, although the primary endpoint (a dose-response effect) was only met in cutaneous lupus erythematosus. Thus, TLR7-TLR8 antagonists might reshape SLE treatment, alone or in combination with other drugs. - Source: PubMed
Publication date: 2026/06/19
Vinuesa Carola GShrotri MadhumitaRahman Anisur - Yellow fever virus (YFV) is a mosquito-borne pathogen causing severe hemorrhagic fever in tropical and subtropical regions. This study aimed to design and evaluated a multi-epitope subunit vaccine against yellow fever virus using immunoinformatics and computational approaches. - Source: PubMed
Publication date: 2026/06/18
Naveed MuhammadAsim MuhammadAziz TariqToheed MuhammadAthar AroosaMajeed Muhammad NoumanKhan Ayaz AliAlharbi MahaShami AshwagAlwethaynani Maher SAlmsaud Mai MAl-Joufi Fakhria A - Obesity remains a major public health challenge, and the contribution of tryptophan metabolism to obesity-associated inflammation remains incompletely understood. Here, we integrated bulk transcriptomic and single-cell RNA sequencing datasets from the Gene Expression Omnibus (GSE25401, GSE217007, GSE166047, and GSE176171) with a curated set of tryptophan metabolism-related genes. Weighted gene co-expression network analysis and differential expression analysis identified 95 differentially expressed tryptophan metabolism-related genes. Protein-protein interaction analysis, univariate logistic regression, and machine-learning models including random forest, support vector machine, and generalized linear model prioritized five biomarkers: SPI1, ITGB2, CD86, CYBB, and TLR8. All five genes were upregulated in obesity and were enriched in immune-related pathways. Single-cell analysis identified major adipose tissue cell populations and showed that SPI1, CD86, CYBB, and TLR8 were predominantly expressed in monocytes, whereas ITGB2 was enriched in natural killer cells. Immune infiltration analysis further supported close associations between these biomarkers and obesity-related immune dysregulation. RT-qPCR validation confirmed increased expression of ITGB2, CD86, and SPI1 in adipose tissue from obese individuals, whereas CYBB and TLR8 were not significantly different between groups. Together, these findings identify tryptophan metabolism-linked biomarkers associated with obesity and suggest that their main translational relevance may lie in stratifying or targeting obesity-associated secondary inflammation. - Source: PubMed
Publication date: 2026/06/18
Zhang YiyiPeng BoZhu YingZhou Hui - The fourth LBMR-Tim (Toulouse Referral Medical Laboratory of Immunology) symposium was convened on December 15th, 2025, in Toulouse, France, to discuss recent advances in the understanding and management of systemic sclerosis (SSc) and systemic lupus erythematosus (SLE). Pathophysiological mechanisms underlying SSc and SLE were discussed from a genetic perspective, with particular emphasis on the X-chromosomal / locus and the interferon signaling pathway. Cellular aspects were explored, highlighting the critical roles of regulatory T cells (Tregs), exhausted T cells, macrophage polarization, and endothelial cells. At the translational research frontier, significant initiatives are underway within the framework of the European Autoimmunity Standardization Initiative (EASI) aimed at enhancing routine biomarker application for diagnosis, disease monitoring, and prognostic considerations. Emerging biomarker candidates promise potential for improving prognostic assessment and follow-up in lupus nephritis (e.g., urinary sCD163/creatinine ratio), cardiovascular complications and vasculopathy associated with SSc (e.g., dephosphorylated-uncarboxylated matrix Gla protein [dp-ucMGP] and endothelial progenitor cells), as well as therapeutic response evaluation (e.g., IGRA-PHA assays and proteomic methodologies). Therapeutically, a paradigm shift is underway with the development of efficacious mono- and multi-targeted antibody treatments alongside cellular therapies designed to eliminate B cells through chimeric antigen receptor (CAR) T cells or to re-establish immune regulation through Treg restoration. The integration of these therapeutic modalities necessitates further investigation to optimize individualized patient selection and management strategies. The multidisciplinary expert panel advocates for a comprehensive approach encompassing fundamental science, translational research, clinical expertise, and therapeutic innovation to advance in the management of these two complex syndromes. - Source: PubMed
Publication date: 2026/06/05
Renaudineau YvesHedrich Christian MGuery Jean-CharlesMiyara MakotoDamoiseaux JanMouthon LucPugnet GregoryFaguer StanislasDelpuech AntoineBellière JulieSailler LaurentPuissant BénédicteFusaro Mathieu - SARS-CoV-2 infection causes an innate immune response that is activated through pattern-recognition receptors (PRRs), including Toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs). Endosomal TLR7/8 detects viral ssRNA, while TLR3 also recognizes dsRNA formed during viral replication. Both RIG-I and MDA5 recognize SARS-CoV-2 RNA in the cytoplasm of infected cells. PRR pathways recruit essential downstream adapter proteins to induce type I interferons (IFNs) and inflammatory cytokines. While genetic variations in host may influence SARS-CoV-2 infection, immune response, and COVID-19 severity, their specific role in triggering these processes remains unclear. This study analyzes the frequency of specific polymorphisms within genes in COVID-19 patients to evaluate their impact on disease severity. - Source: PubMed
Publication date: 2026/05/28
Paradowska EdytaKania Katarzyna DJarych DariuszMikulski DamianJabłonowska ElżbietaHaręża Daria AWójcik-Cichy Kamila