TLR2
- Known as:
- TLR2
- Catalog number:
- 000136A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- TLR2
Related genes to: TLR2
- 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
Related articles to: TLR2
- Acute ischaemic stroke (AIS) remains a leading cause of death and disability. This exploratory study integrated transcriptomic and metabolomic analyses to identify candidate hub genes and metabolites associated with AIS and to provide preliminary insights into its molecular mechanisms and potential therapeutic targets. - Source: PubMed
Publication date: 2026/04/15
Zhang JiayanZhou XinHe Dian - Breast cancer is a common cancer type that occurs among women in Pakistan, and the rising incidence and mortality rate underline the need to develop effective, patient-tailored immunotherapies. In this study, we implemented an end-to-end immunoinformatics workflow using publicly available whole-exome sequencing (WES) data deposited under NCBI BioProject PRJNA941166, a cohort-derived resource from the Khyber Pakhtunkhwa region; as a proof of concept, we analyzed all sequencing runs associated with the available case to demonstrate a personalized vaccine design workflow. Somatic variant analysis indicated a high mutational burden, including 6005 missense mutations in genes such as MUC3A and TTN. From > 43,000 candidate mutant peptides, we prioritized seven non-allergenic neoantigens with strong predicted HLA binding (ΔG ≤ - 13.0 kcal/mol). These epitopes were assembled into a 285-amino acid multi-epitope antigen incorporating a GM-CSF adjuvant and helper epitopes. AlphaFold2 modeling and in silico quality assessment supported construct stability (ProSA Z-score - 7.14; ERRAT 96.59%). Across 500 ns molecular dynamics simulations, the vaccine construct remained conformationally stable and showed favorable predicted interactions with innate immune receptors, with strong binding free energies for TLR9 (ΔG = - 148.8 kcal/mol) and TLR2 (ΔG = - 16.7 kcal/mol). Immune simulations using C-IMMSIM suggested a Th1-skewed response characterized by induction of cytotoxic T lymphocytes, memory T-cell formation, and elevated IFN-γ. Although limited to computational predictions and a single publicly available case, the predicted receptor engagement and immunogenicity provide a rationale for preclinical evaluation of this personalized mRNA vaccine design workflow in high-risk populations. - Source: PubMed
Publication date: 2026/04/28
Raheem KayodeNawaz MariyamAlzahrani Khalid JAli IjazMuddassar Muhammad - Nipah virus (NiV) remains a critical zoonotic threat in South and Southeast Asia due to its high fatality rate and the absence of a licensed human vaccine. In this study, an immunoinformatics-driven strategy was employed to design a population-specific multi-epitope vaccine targeting the fusion (F) and glycoprotein (G) of NiV. A total of four B-cell epitopes, ten cytotoxic T lymphocyte (CTL) epitopes, and eight helper T lymphocyte (HTL) epitopes were selected based on strong HLA binding affinity, high antigenicity, and favorable safety profiles. All selected epitopes were predicted to be non-allergenic and non-toxic, with VaxiJen antigenicity. Population coverage analysis revealed extensive coverage across endemic regions, exceeding 97.98% in South Asia and 99.41% in Southeast Asia. The final multi-epitope construct demonstrated favorable physicochemical properties, including structural stability and hydrophilic characteristics. Structural modeling and validation confirmed a reliable tertiary structure, with 92.2% of residues located in favored regions of the Ramachandran plot and an ERRAT score of 90.5. Molecular docking analysis showed strong binding affinities between the vaccine construct and Toll-like receptors, particularly TLR3 (-17.0 ΔG kcal/mol, 8 hydrogen bonds, 7 salt bridges), followed by TLR4 (-15.8 ΔG kcal/mol, 14 hydrogen bonds, 3 salt bridges) and TLR2 (-15.1 ΔG kcal/mol, 10 hydrogen bonds, 3 salt bridges), suggesting a potential for innate immune receptor engagement that warrants further experimental validation. Structure-based flexibility analyses suggested limited conformational fluctuations at the predicted vaccine-receptor interaction interfaces. Immune simulation predicted robust humoral and cellular immune responses, characterized by elevated IgG titers, cytokine production, and the generation of memory B and T cells. Codon optimization and in silico cloning into the pET-28a(+) vector indicated high expression feasibility in K12. Overall, this study presents a rational computational framework for developing a safe, immunogenic, and region-specific NiV vaccine candidate, warranting further experimental validation. - Source: PubMed
Publication date: 2026/04/28
Afnani Moh RoyhanKharisma Viol DheaKhairullah Aswin RafifAbdurasulov AbduganiAbdyldayeva RozaRebezov MaksimParikesit Arli AdityaJakhmola VikashRollando RollandoAnsori Arif Nur Muhammad - Acute Lymphoblastic Leukemia (ALL) remains the most prevalent childhood malignancy. While chemotherapy has improved survival rates, multidrug resistance (MDR) mediated by P-glycoprotein (P-gp/ABCB1) overexpression persists as a major cause of treatment failure and relapse. Natural Killer (NK) cells are pivotal for anti-leukemic surveillance but are often compromised during treatment due to their susceptibility to chemotherapy, a vulnerability intrinsically linked to their own expression of P-gp. Strategies to transiently enhance NK cell chemoresistance could therefore preserve immune function and improve therapeutic outcomes. We hypothesized that stimulating Toll-Like Receptor 2 (TLR2) on NK cells could modulate P-gp expression or activity, enhancing their resilience to cytotoxic drugs. - Source: PubMed
Publication date: 2026/04/15
Álvarez-Carrasco PabloBasurto-Olvera PaolaJiménez-Hernández ElvaMedina-Sanson AuroraMaldonado-Bernal Carmen - Generalized canine demodicosis caused by Demodex canis is a chronic parasitic dermatosis associated with immune dysregulation; however, the integrated molecular mechanisms underlying host-parasite interaction remain incompletely characterized. The present study investigated systemic innate and adaptive immune gene expression in dogs with generalized demodicosis compared with healthy controls using quantitative real-time PCR (qRT-PCR). Peripheral blood mononuclear cells (PBMCs) were isolated from 18 dogs with generalized demodicosis and six clinically healthy dogs. Relative mRNA expression of Toll-like receptors (TLR2, TLR6, TLR9), cytokines (IL4, IL5, IL10, IL13, IFNG, TGFB1), and the inflammasome-related gene NLRP3 was quantified and normalized to GAPDH. Dogs with generalized demodicosis showed significant upregulation of TLR2 (P = 0.030), TLR6 (P = 0.008), IL4 (P = 0.029), IL5 (P = 0.025), IL10 (P = 0.003), IL13 (P = 0.031), and NLRP3 (P = 0.001), genes along with significant downregulation of TLR9 (P = 0.014) and IFNG (P = 0.004) genes. TGFB1 gene expression was upregulated but not statistically significant. These findings demonstrate coordinated modulation of innate receptor signaling, Th2-skewed cytokine polarization, suppression of Th1-mediated immunity, and enhanced inflammasome priming in generalized demodicosis. The study provides integrated molecular evidence that generalized canine demodicosis represents a systemic immune dysregulation disorder rather than a purely localized parasitic overgrowth. - Source: PubMed
Publication date: 2026/04/28
Dawar PoojaSingh Shanker KSrivastava Mukesh KumarKumari PriyambadaYadav BrijeshKumari ReetuKumari SanjuVerma KrishnaHasan MohdSingh AnjaliTomar Prerna