TLR2 Blocking Peptide (N-terminal)
- Known as:
- TLR2 Blocking Peptide (N-terminal)
- Catalog number:
- 33r-11063
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- TLR2 Blocking Peptide (N-terminal)
Related genes to: TLR2 Blocking Peptide (N-terminal)
- 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 Blocking Peptide (N-terminal)
Related articles to: TLR2 Blocking Peptide (N-terminal)
- 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 - Immune checkpoint inhibitors are a frontline treatment for metastatic renal cell carcinoma (RCC), one of the most common malignancies of the urinary system. However, a large proportion of patients exhibit poor responses or develop resistance, which severely limits the therapeutic efficacy and patient survival. In this study, we constructed a custom CRISPR activation library based on the top 500 genes upregulated in anti-PD-1-resistant RCC cells. Functional screening identified serum amyloid A1 (SAA1) as a critical mediator of resistance; SAA1 activation promoted immune evasion, while deficiency sensitized RCC cells to anti-PD-1 treatment. SAA1 promoted anti-PD-1 resistance both in RCC patients and in mouse models. Mechanistically, SAA1 bound to toll-like receptor 2 (TLR2) and activated the NF-κB signaling pathway, thereby inducing the formation of neutrophil extracellular traps (NETs). These NETs not only acted as physical barriers that blocked direct contact between CD8⁺ T cells and tumor cells but also promoted CD8⁺ T cell exhaustion, facilitating tumor immune evasion and resistance to immunotherapy. Both in vitro and in vivo experiments demonstrated that suppression of SAA1 significantly reduced NET formation and enhanced the efficacy of immunotherapy. In conclusion, SAA1 promotes immunotherapy resistance in RCC by driving NET formation via the TLR2/NF-κB axis and inducing CD8⁺ T cell dysfunction. Targeting SAA1 may represent a promising strategy to overcome immune resistance in RCC. - Source: PubMed
Publication date: 2026/04/30
Luo XinZou XiangpengWu YiWen Jun-HuaLuo YunhanYang XiaofengZhou ZhaohuiXiong LongbinNing KangYe BaokuiZhang LihaoLin YisongJiang BiaoZhang ZhuoqiZhou FangjianDong PeiYu ChunpingPeng YuluZhang Zhiling - Building on our previous research, which classified Kikuchi disease into three subtypes based on predominant symptoms and fever status - febrile type, febrile lymphadenopathy (FebLAP), and afebrile lymphadenopathy (aLAP) - we further investigated the underlying mechanisms contributing to their distinct clinical differences. Using NanoString nCounter technology, we analyzed the gene expression profiles of 35 Kikuchi disease lymph node specimens and compared them across the subtypes. Compared with the febrile type, aLAP exhibited higher AICDA expression, a trend observed in both germinal center positive and negative cases. The aLAP specimens also showed higher expression of B-cell markers; however, CD20 immunohistochemical staining did not reveal an increased number of B cells in aLAP. We therefore hypothesize that aLAP contains a higher proportion of atypical memory B cells, characterized by elevated AICDA and B-cell marker expression compared with other B-cell subsets. Immunohistochemical staining demonstrated that IRTA1+ atypical memory B cells were present in 64% (23/36) of aLAP cases, significantly higher than in FebLAP (0/8, 0%) and the febrile type (2/11, 18%) (p < 0.001). This finding confirms that aLAP is more likely to contain atypical memory B cells compared with the other subtypes. Pathway analysis revealed that the febrile type upregulates pathways associated with TLR2 and TLR4 signaling and neutrophil degranulation, while aLAP upregulates the TNFR2 non-canonical NF-κB pathway. RNAscope in situ hybridization demonstrated higher TLR4 expression in the febrile type compared with the aLAP type. These findings suggest that the triggering microbes for each subtype may differ, leading to distinct immune responses and clinical presentations. Overall, these results provide new insights into the immunopathogenesis of Kikuchi disease and highlight the potential role of atypical memory B cells in shaping its distinct clinical presentations. © 2026 The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/04/29
Yu Shan-ChiChang Kung-ChaoChen Tseng-ChengChen Chun-NanYang Tsung-Lin - Positive and balancing selection on pattern recognition receptors (PRRs) is widely thought to target ligand-binding domains and affect the specificity of recognition of different pathogens. Alternatively, positive/balancing selection on PRRs could affect general responsiveness by targeting for example signaling domains or cis-regulatory variation. Studies of a wild rodent (the bank vole, Clethrionomys glareolus) have shown that Tlr2-a lipoprotein-binding PRR-is highly polymorphic with divergent haplotypes and signatures of balancing selection, and that Tlr2 genotype is associated with susceptibility to Borrelia afzelii infection in the wild. To investigate what aspect of Tlr2 function has been under selection, we here perform integrated population genetic and functional analyses. Ex vivo infection experiments show that the protective Tlr2 haplotype produces a stronger proinflammatory response to B. afzelii compared to the haplotype associated with susceptibility. Tlr2 genotype has a similar, albeit not statistically significant, effect on responsiveness to the phylogenetically distant pathogen Streptococcus pyogenes. We find that the strongest signature of balancing selection is 4.6 kb upstream of the Tlr2 coding sequence, near a putative enhancer, and that Tlr2 exhibits allele-specific expression such that the protective haplotype is more expressed. Collectively these results indicate that balancing selection has primarily acted on cis-regulatory variation affecting the general responsiveness via Tlr2-signaling rather than on polymorphisms affecting Tlr2 ligand-binding specificity. - Source: PubMed
Publication date: 2026/04/29
Nandakumar MridulaLundberg MaxNouri MehrnazValfridsson ChristineCarlsson FredricRåberg Lars - Human periodontal ligament fibroblasts (PDLFs) can acquire osteoblast-like characteristics within periodontal lesions and contribute to osteoclastogenesis through the expression of receptor activator of nuclear factor (NF) κB ligand (RANKL). However, the microbial and cellular conditions required for RANKL induction remain unclear. This study compared the microbial responsiveness of undifferentiated and osteoblast-like PDLFs to clarify the mechanisms regulating RANKL expression. - Source: PubMed
Abe MasayoKamijyo KoheiOda ShintaroSakagami HiroshiHayashi JoichiroInomata Megumi