Ask about this productRelated genes to: TLR9 antibody
- Gene:
- TLR9 NIH gene
- Name:
- toll like receptor 9
- Previous symbol:
- -
- Synonyms:
- CD289
- Chromosome:
- 3p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-27
- Date modifiied:
- 2016-10-05
Related products to: TLR9 antibody
Related articles to: TLR9 antibody
- While injectable vaccines can prevent respiratory pathogens from causing severe disease, their ability to elicit protective local immunity in the respiratory mucosa is more limited. For viral pathogens, infection outcome is often determined at the site of entry, where innate immune sensing within the airway mucosa precedes and conditions adaptive immune responses. At these surfaces, epithelial cells and antigen-presenting cells express a wide repertoire of pattern recognition receptors (PRRs), positioning innate immune activation as a central determinant of vaccine efficacy and durability of mucosal immunity. Recent advances in mucosal immunology facilitate the progression of mucosal vaccine development from empirical formulation toward mechanism-informed targeting of innate immune pathways. This review highlights emerging evidence supporting targeted engagement of cytosolic and endosomal PRRs to enhance intranasal vaccine efficacy. We focus on the cyclic GMP-AMP synthase-stimulator of interferon genes (STING) pathway, highlighting how spatially and temporally constrained STING activation can drive interferon-mediated antiviral immunity, enhance antigen presentation and promote tissue-resident T cells. We also discuss how complementary targeting of endosomal PRRs, including TLR3 and TLR9, further reinforces antiviral programming and adaptive immunity at mucosal sites. - Source: PubMed
Publication date: 2026/04/22
Dederko Dorian CLavelle Ed C - Recalcitrant airway inflammatory diseases have drawn significant attention due to their high incidence and substantial healthcare costs. Analysis of clinical samples from patients with chronic rhinosinusitis with nasal polyps (CRSwNP) revealed the coexistence of neutrophilic and eosinophilic inflammation, which may account for the limited efficacy of traditional single-target therapeutic strategies. Moreover, cell-free DNA (cfDNA)-an emerging inflammatory mediator-has been implicated in both eosinophilic and neutrophilic responses through its role in the formation of extracellular traps. In this study, we developed tannic acid (TA)-modified CuInPS (CIPS) nanosheets (C-TA; w/w = 1:1) as a multi-targeting therapeutic nanoplatform for recalcitrant airway inflammatory diseases. The C-TA nanosheets demonstrated efficient cfDNA clearance via hydrogen bonding interactions, thereby inhibiting cfDNA-triggered toll-like receptor 9 (TLR9) activation and subsequent nuclear factor-κB (NF-κB) inflammatory signaling. Additionally, C-TA exhibited potent antioxidant and antibacterial activities, which were ascribed to the inherent properties of the two-dimensional nanostructure and the chemical characteristics of TA, respectively. The in vivo therapeutic efficacy of C-TA was evaluated in murine models with neutrophilic and eosinophilic airway inflammation, respectively. C-TA markedly attenuated airway inflammation in both of these animal models by reducing reactive species, immune cell infiltration, goblet cell hyperplasia and the expression of pro‑inflammatory cytokines. Furthermore, treatment with C-TA effectively modulated the dysregulated airway microbiota observed in the inflammatory state. Our findings demonstrate a multi-targeting nanoformulation designed to mitigate multiple key pathological drivers of severe airway inflammation concurrently. This engineered system presents a promising strategy for managing respiratory inflammatory disorders and also other inflammation-related diseases. - Source: PubMed
Publication date: 2026/03/12
Liu MingXu ChangyiMa RenqiangXie XinranXie YingDu MengyaXu ZhaofengZhang ShuaiyinLi JianWen WeipingTu Zhaoxu - Current mRNA-LNP systems face challenges in efficient co-delivery of nucleic acid adjuvants, limiting their capacity to elicit robust cellular immunity. To overcome the dissociation limitations of physically admixed CpG in conventional lipid nanoparticles, we developed a covalent conjugation platform that integrates TLR9 agonists with phospholipids via amide bonding. We synthesized a DSPE-CpG conjugate, which exhibited high loading efficiency (97.1%) onto mRNA-LNPs. The immune activation efficacy was evaluated in models encoding SARS-CoV-2 spike protein and HBV antigens. The DSPE-CpG-mRNA LNP system demonstrated enhanced cellular uptake via clathrin-mediated endocytosis, superior lymph node targeting of the adjuvant, and improved antigen expression in vivo. In the SARS-CoV-2 model, it induced high levels of IFN-γ⁺CD8⁺ T cells and elicited higher titers of specific IgG and neutralizing antibodies. In the HBV model, it significantly enhanced antigen-specific CD107a and FasL CTLs. Acute toxicity tests revealed no significant adverse effects. This covalent conjugation strategy, by ensuring co-localized delivery of antigen and adjuvant, provides an innovative and translatable platform for enhancing mRNA vaccine efficacy. - Source: PubMed
Publication date: 2026/04/17
Ji WantingZhu KeerZhou YanyanYan HaominWei JianiZhu YingLi ShengHong YuqiDai JinyaoDong ShaohuaHu HaoyangYou JianQiu YunqingLou Yan - Extracellular histones, once regarded solely as nuclear structural proteins, are now recognized as potent mediators of thrombo-inflammation which is the pathological interface of coagulation and immunity. Released during necrosis, apoptosis, and neutrophil extracellular trap (NET) formation, histones act as damage-associated molecular patterns (DAMPs), engaging receptors such as Toll-like receptors (TLR2, TLR4, TLR9) to trigger endothelial dysfunction, platelet activation, and cytokine release. Post-translational modifications (PTMs), including citrullination, acetylation, and methylation, further modulate histone immunogenicity, cytotoxicity, and procoagulant potential. These mechanisms amplify thrombin generation, impair anticoagulant pathways, and promote vascular permeability, positioning histones as central drivers of immunothrombosis in sepsis, stroke, ARDS, COVID-19, and autoimmune disorders. Circulating histones and nucleosomes are emerging as biomarkers for disease severity and prognosis. Therapeutic strategies targeting histones, such as neutralizing antibodies, heparin derivatives, PAD inhibitors, and activated protein C, show promise in mitigating histone-driven pathology. This review highlights mechanistic insights into histone biology and explores translational opportunities for targeted interventions at the intersection of inflammation and thrombosis. - Source: PubMed
Publication date: 2026/04/01
Mohiuddin NailaShah YeshaSubramaniam Saravanan - Angiotensin II (AngII) causes hypertension and vascular inflammation and is essential in neurohumoral activation promoting the development of heart failure. The role of the adaptor protein myeloid factor of differentiation 88 (MyD88) driving this pathology remains incompletely understood. - Source: PubMed
Publication date: 2026/02/27
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