Anti-Mouse CD282 (TLR2) FITC 25 ug
- Known as:
- Antibody toMouse CD282 (TLR2) fluorecein 25 ug
- Catalog number:
- 11-9022-80
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD282 (TLR2) FITC 25
Related genes to: Anti-Mouse CD282 (TLR2) FITC 25 ug
- Gene:
- TLR2 NIH gene
- Name:
- toll like receptor 2
- Previous symbol:
- -
- Synonyms:
- TIL4, CD282
- Chromosome:
- 4q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-25
- Date modifiied:
- 2016-10-25
Related products to: Anti-Mouse CD282 (TLR2) FITC 25 ug
Related articles to: Anti-Mouse CD282 (TLR2) FITC 25 ug
- Nosocomial pulmonary infection is a frequent complication after spontaneous intracerebral hemorrhage and may worsen neurological recovery, prolong hospitalization, and increase clinical burden. This retrospective clinical-laboratory study presents a reproducible workflow for evaluating inflammatory biomarker and host immune-genetic profiles associated with nosocomial pulmonary infection after primary spontaneous intracerebral hemorrhage. Patients are classified according to whether nosocomial pulmonary infection occurs after admission. Peripheral venous blood is collected in the early post-admission period under standardized pre-analytical conditions. Serum is separated, aliquoted, and stored for enzyme-linked immunosorbent assay measurement of IL-1β, IL-6, IL-10, IL-17, IFN-γ, TNF-α, TLR2, TLR4, and TLR9. In parallel, genomic DNA is extracted from anticoagulated whole blood and used for polymerase chain reaction-restriction fragment length polymorphism genotyping of selected cytokine- and Toll-like receptor-related loci. The workflow also includes quality-control procedures for sample handling, duplicate ELISA measurements, DNA purity assessment, genotype calling, and repeat genotyping. Statistical analysis includes between-group comparison of clinical characteristics and biomarker levels, Hardy-Weinberg equilibrium testing, logistic regression analysis for genotype and allele associations, adjustment for relevant clinical covariates, and false-discovery-rate correction for multiple genetic comparisons. This combined clinical, inflammatory, and immune-genetic workflow may help characterize infection-risk profiles after spontaneous intracerebral hemorrhage, although prospective multicenter validation is still required before routine clinical application. - Source: PubMed
Publication date: 2026/08/04
Yang LunyunZhou HuiLi WeiShen Weifeng - Diabetic foot ulcers (DFUs) often exhibit impaired healing. Macrophage imbalance driven by persistent inflammation is one contributing factor, with a predominance of inflammatory over anti-inflammatory macrophages in non-healing ulcers. Monocytes, precursors of macrophages, are skewed towards an inflammatory phenotype in diabetes. Here, we investigated whether monocyte inflammatory skewing is further exacerbated in individuals with DFUs and explored how it relates to an individual's metabolic (HbA1c and lipids) profile. Monocyte inflammatory profile was assessed by examining phenotypic markers, gene expression, and cytokine production. We observed an elevation in total monocytes and the intermediate subset in the DFU group compared with healthy individuals. In addition, an impaired monocyte profile was seen in the DFU group, with a suppression of both inflammatory (CD86, TLR2, and TLR4) and anti-inflammatory (CD163) markers, accompanied by the downregulation of distinct inflammatory and anti-inflammatory genes. Despite a suppressed phenotype, DFU monocytes showed an increased basal TNF and IFN-γ production, indicating low-grade inflammation. Further, in exploratory analysis, monocyte CD86 and CD163 inversely correlated with HbA1c, while CD163 negatively correlated with cholesterol/HDL-C and triglycerides, suggesting links between metabolic control and monocyte phenotype. Taken together, the impaired monocyte profile indicates underlying pathogenic inflammation and monocyte dysfunction in people with DFUs, suggesting the monocyte profile could serve as a potential biomarker for immunomodulation in DFU. - Source: PubMed
Marimuthu RekhaMedbury Heather JBaraz RanaVicaretti MauroLau Sue-LynnGunton Jenny ELi StephenWilliams Helen - This narrative review aimed to critically synthesize and evaluate the current evidence on the roles of TIR domain-containing adaptor protein in tumorigenesis and cancer progression, with a particular focus on elucidating the underlying inflammatory and immune regulatory mechanisms mediated by toll-like receptor signaling. A targeted literature search of recent studies (2015-2024) was performed using PubMed and Web of Science. Classic foundational publications (1998-2014) were supplemented through reference tracking. We included experimental, cellular, and clinical studies focusing on TIR domain-containing adaptor protein in cancer. The synthesized findings indicate that TIR domain-containing adaptor protein has been implicated in malignant progression in bladder, pancreatic, and gastric cancers by sustaining chronic inflammation and shaping an immunosuppressive tumor microenvironment through the TLR2/4-MyD88-NF-κB/MAPK axis, whereas it may exert homeostatic and protective effects in colorectal cancer. TIR domain-containing adaptor protein activity is tightly regulated by cellular origin, ligand specificity, and epigenetic modifications such as promoter methylation, which are closely associated with cancer risk and disease severity. TIR domain-containing adaptor protein serves as a critical regulator in inflammation-driven tumors with distinct context-dependent functions and represents a promising biomarker and therapeutic target. Further research focusing on its precise regulatory mechanisms and cell-specific targeted strategies will facilitate its clinical translation. - Source: PubMed
Publication date: 2026/08/17
Jiang HuihuiZhang RuiDing ShanshanYu ZhenQi ChenruiMeng JinWang Lu - Neurological disorders are a major global health challenge in the current era, and they need new therapeutic treatments. - Source: PubMed
Al Hasan Md SakibShahria NazninEmon YasinAlshahrani Mohammad YMia EmonAltemani Faisal HSuma Rituparna BiswasSumaya Umme HabibaUddin Mohammed BurhanIslam Md Torequl - Unlike adult hearts, neonatal hearts can regenerate and adapt to stress. To identify both cardioprotective and regenerative mechanisms, we compared activated genes and related signaling pathways in the neonatal mouse heart after myocardial infarction (MI) and after exposure to pressure overload using a neonatal model of transverse aortic constriction (nTAC) at postnatal day 1 (P1). We identified three immune-related genes-Ccl4, S100a8, and C1qa-of high interest, as they encode secreted factors, are highly expressed in the neonatal mouse heart in both injury types, and their receptors are expressed on neonatal cardiomyocytes (nCM) and cardiac endothelial cells (EC). We investigated their effects on primary mouse EC and nCM in vitro. Our study found that the combination of these secreted factors (Pool3) enhances EC and nCM cell cycle re-entry and reduces the rate of apoptosis. Combined in vivo and in vitro transcriptome analyses revealed that Toll-like receptor 2 (TLR2) activation in nCM induces a shared pro-survival and cell cycle re-entry-associated signaling, including upregulation of Bcl2 and Birc5, respectively. The direct and pivotal role of TLR2 in enhancing nCM cell cycle re-entry and survival was further confirmed using TLR2 knockout (KO) nCM, a TLR2 inhibitor, and a TLR2 agonist (zymosan). Moreover, the importance of TLR2 in mediating the adaptive response to pressure overload in neonatal mice was confirmed in TLR2 KO mice, which failed to adapt to pressure overload and exhibited high mortality together with maladaptive cardiac remodeling as early as 7 days post-surgery. Collectively, these findings demonstrate that TLR2 is essential for mediating nCM cell cycle re-entry, survival, and adaptive/regenerative response to injury. - Source: PubMed
Publication date: 2026/08/14
Nicke JuliaGoldspink AdrianMenn MalteFleischmann Bernd KMalek Mohammadi Mona