TLR9 Antibody
- Known as:
- TLR9 Antibody
- Catalog number:
- XW-7626
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- TLR9 Antibody
Related 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
- Innate immune receptors are central to host resistance against Trypanosoma cruzi infection, yet how parasite genetic diversity is associated with these responses remains poorly understood. Here, we characterized acute infection outcomes and myocardial innate immune transcriptional profiles in mice subjected to single and mixed infections with genetically distinct T. cruzi parasites (DTUs TcII, TcIII, and TcVI). Swiss mice were infected with RN2, RN23, Y, or CL-Brener individually or in combination, and parasitemia, survival, and cardiac gene expression were assessed. The Y strain, CL-Brener clone, and RN2 + RN23 + CL-Brener condition exhibited a high-severity profile, with marked parasitemia (8000-28,000 trypomastigotes/5 μL), mortality of 74%-100%, reduced myocardial transcription of Tlr2, Tlr4, Tlr9, Trif, and Myd88, and increased transcription of Nlrp3, Casp1, Il1β, and Tnfα. In contrast, RN2 and RN23 single infections exhibited low-severity profiles and higher transcription of innate immune mediators associated with parasite control. Mixed-infection groups displayed transcriptional and infection profiles differing from the corresponding single-infection groups under a standardized total inoculum. Together, these findings identify distinct myocardial innate immune transcriptional profiles across single and mixed T. cruzi infection conditions and support further investigation of the contributions of parasite population composition and dose to acute infection outcomes. - Source: PubMed
Sampaio George Harisson FelintoBarbosa-Silva Andressa Noronhado Nascimento Brito Carlos RamonBatista Lucas Abrantesde Negreiros Christiane Carlos Araújode Medeiros Brito Ramayana MoraisMartins Rand RandallNascimento Manuela Sales Limada Câmara Antonia Claudia Jácomeda Matta Guedes Paulo Marcosda Cunha Galvão Lúcia Maria - B-cell receptor (BCR) inhibitors have transformed chronic lymphocytic leukemia (CLL) therapy, yet many patients show incomplete responses or develop resistance in the absence of Bruton's tyrosine kinase (BTK) mutations. We investigated Toll-like receptor 9 (TLR9) signaling as a tumor-response mechanism to BCR blockade. Using 102 TLR9-stimulated patient samples, we identified two distinct migratory phenotypes: TLR9-induced migratory Responders (R), with enhanced migration, and TLR9-induced migratory Reverse-Responders (RR), with suppression of migration following TLR9 activation. Transcriptomic and protein analyses showed TLR9-stimulated R samples expressed higher IRAK4/IRAK1 and induced NF-kB p100, consistent with intact TLR9 signaling. In contrast, RR samples exhibited elevated basal BCR activity, and lower IRAK4/IRAK1 with rapid IRAK1 degradation, indicating suppressed TLR9 signaling. In-silico modeling and biochemical validation showed high basal BCR signaling suppresses TLR9 responsiveness, whereas low basal activity permits full TLR9 activation. Functionally, TLR9-induced migration persisted despite BTK inhibition (BTKi) in R but not RR samples, and was abrogated by TLR9 antagonism, consistent with signaling through a BTK-independent pathway in the R subgroup. CLL cells from BTKi-resistant patients expressed higher TLR9 and matched pre- and post-relapse samples showed decreased BCR and increased TLR-associated NF-kB signaling post-relapse. Clinically, in small exploratory. - Source: PubMed
Publication date: 2026/10/05
Kennedy EmmaStott LaurenAshworth IonaLadikou EleniJones John RJohnston RosalyndVareli AimiliaGattei ValterZucchetto AntonellaLiloglou TriantafillosPatten Piers EmJayne SandrineDyer Martin JsGirvan Sean FCairns David ASimoes FabioMitchell SimonPepper ChrisPepper Andrea Gs - Leber hereditary optic neuropathy (LHON) is a mitochondrial disease caused primarily by pathogenic mitochondrial DNA (mtDNA) variants that impair respiratory chain complex I function. Although bioenergetic failure, oxidative stress, and retinal ganglion cell degeneration are central features of disease pathogenesis, these mechanisms do not fully explain the incomplete penetrance, male predominance, and marked clinical heterogeneity observed in LHON. Emerging evidence suggests that mitochondrial dysfunction can also trigger sterile inflammatory responses through the release of mitochondrial damage-associated molecular patterns (DAMPs), including mtDNA and reactive oxygen species, and through impaired mitophagic clearance. These signals activate innate immune pathways, including cGAS-STING, TLR9, and the NLRP3 inflammasome, potentially contributing to neuroinflammation, glial activation, and secondary neuronal injury. The relevance of immune signaling has gained further attention with the development of AAV-based gene therapies for LHON, where treatment-associated ocular inflammation has emerged as a clinically important challenge. In this review, we examine the evidence linking mitochondrial dysfunction to innate immune activation in LHON, discuss the immunological mechanisms underlying disease progression and gene therapy-associated inflammation, and highlight emerging opportunities for biomarker development, immunomodulatory intervention, and improved therapeutic design. We propose that LHON should be viewed not only as a disorder of mitochondrial bioenergetics but also as a neuroinflammatory disease shaped by the interplay between mitochondrial stress and immune signaling. - Source: PubMed
Publication date: 2026/09/18
Zhang XueChang AiqinLiu YuanYu Hong - - Source: PubMed
Publication date: 2026/10/01
- This study aims to systematically investigate the relationship between serum perfluoroalkyl and polyfluoroalkyl substances (PFAS) and chronic obstructive pulmonary disease (COPD), along with its potential mechanisms, through a combination of population analysis and bioinformatics approaches. - Source: PubMed
Publication date: 2026/09/30
Wang JunLi XinHuang Sha