Ask about this productRelated genes to: TLR2 antibody
- 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: TLR2 antibody
Related articles to: TLR2 antibody
- This study investigated the protective effect of zinc supplementation on insulin release via modulation of the High Mobility Group Box 1 (HMGB1)/Toll-like receptor 2 (TLR2)/mitogen-activated protein kinase (MAPK) signaling pathway in streptozotocin (STZ)-induced pancreatic β-cell injury, a commonly used model of type 1 diabetes. - Source: PubMed
Yesildag SahinYılmaz Akyüz ElvanTaskin Eylem - Japanese encephalitis (JE) caused by Japanese encephalitis virus (JEV) infection remains one of the major types of viral encephalitis. The mechanisms underlying JEV infection and pathogenesis have not been fully elucidated, resulting in the absence of specific therapies for JE. Neuronal apoptosis is a well-established outcome of JEV infection; however, its secondary contributions to JE pathogenesis remain largely uncharacterized. Here, we demonstrate that apoptotic bodies (ApoBDs) derived from JEV-infected neurons package infectious JEV particles, facilitating viral transmission between neurons, as well as between neurons and microglia. Further investigations revealed that microglia predominantly internalize the ApoBDs via phagocytosis and dynamin 2-dependent endocytosis. Moreover, lipids, rather than nucleic acids or proteins, are the key pro-inflammatory constituents of ApoBDs. Subsequent studies demonstrated that ApoBDs activate microglia through the TLR2/TLR4-NF‑κB signalling. In vivo experiments showed that JEV-loaded ApoBDs elicit significantly more severe neuroinflammation and pathological lesions compared to ApoBD-free virions. These findings underscore the non-negligible contribution of neuron-derived ApoBDs to JEV pathogenesis, providing valuable insights for the development of novel therapeutic strategies against JE. - Source: PubMed
Zeng ChuanNan XiaoweiWang TingXiong JunyaoZhu ShuoYang ChengjieZhu BiboSi YouhuiCao ShengboYe Jing - Chronic migraine (CM) is a disabling neurological disorder associated with substantial impairment of quality of life. Increasing evidence suggests that inflammatory and epigenetic mechanisms may contribute to migraine pathophysiology. miR-146, a microRNA involved in the TLR-4/NFkb pathway, is known to regulate proinflammatory signaling, whereas HMGB1 activates inflammatory pathways through TLR2 and TLR4 receptors. IL-17 is another proinflammatory cytokine implicated in both inflammation and cognitive processes. In this research, our aim was to investigate the relationship between serum HMGB1, IL-17, and miR-146 levels and migraine-related subjective cognitive symptoms in patients with CM. - Source: PubMed
Publication date: 2026/06/07
Gök Dağidir HaleBandirmali DuyguCeren Akgör Merve HilalVuralli DoğaYalinay MeltemGümüş Akay GüvemBolay Hayrunnisa - is a significant zoonotic pathogen responsible for severe disease in immunocompromised individuals, adverse pregnancy outcomes, and substantial economic losses in the livestock industry. Given the limitations of current therapeutic strategies and vaccines, this study utilized immunoinformatics and reverse vaccinology approaches to design a multi-epitope candidate vaccine. - Source: PubMed
Publication date: 2026/08/17
Yi ChenchenShen YuLuo YeWang QinTong Xiaomei - Mastitis is a major inflammatory disorder of the mammary gland that causes substantial economic losses in the dairy industry, with Staphylococcus aureus (S. aureus) being one of the predominant causative pathogens. The current treatment options are limited by antimicrobial resistance and drug residues. Therefore, alternative therapeutic strategies are needed. The present study aimed to evaluate the anti-inflammatory and antioxidant effects of an ethnoveterinary oil (EO) formulation in an experimental model of S. aureus-induced mastitis. The EO formulation was prepared according to a standardized traditional ethnoveterinary composition. Mastitis was induced in healthy lactating primiparous Wistar rats by intramammary infusion of S. aureus (2 × 10 CFU/mL), and the twenty-four female Wistar rats were divided into four groups of 6: normal control (NC), mastitis control (MT), standard drug-treated (MT + DEX), and MT + EO-treated groups. The chemical composition of EO was characterized by GC-MS analysis, which identified 21 bioactive compounds, predominantly erucic acid, along with phenolic compounds, fatty acid derivatives, terpenoids, and steroidal constituents known for their anti-inflammatory potential. Biochemical analyses revealed that EO significantly restored endogenous antioxidant enzyme activities and reduced lipid peroxidation in mammary tissues. Furthermore, EO significantly decreased myeloperoxidase (MPO) levels and N-acetyl-β-D-glucosaminidase activity, indicating reduced neutrophil infiltration and protection against epithelial cell damage. The levels of Pro-inflammatory cytokines were markedly elevated in mastitis control group whereas EO treatment significantly suppressed their production. In addition, EO downregulated the gene expression of Toll like receptor-2 (TLR-2) and Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX-2), suggesting modulation of key inflammatory and oxidative stress-related pathways. Histopathological and special staining analyses further confirmed the preservation of mammary gland architecture and attenuation of inflammatory infiltration following EO treatment. Collectively, these findings demonstrate that EO exerts potent anti-mastitic effects through the combined modulation of oxidative stress and inflammatory responses and may serve as a promising natural therapeutic alternative for the management of S. aureus associated mastitis in Wistar rat model. - Source: PubMed
Publication date: 2026/08/30
Ratheesh MJose Svenia PSheethal SSandya SDhar ParulPandit Deeksha