TLR3 (Toll Like Receptor 3)

An extensively comparative molecular dynamics study of the free state and bound states of the two constructs unveiled a more stable interaction, complex stability and immune response attributing to the specificity of the minibinder-based construct towards TLR3. Our work circumscribes a multi-headed approach beginning with peptide subunit multi-epitope vaccine construct design for mitigating mCRPC; secondarily, endorsing the advocacy of TLR3-agonizing minibinders as vaccine adjuvants for enhanced immunity and finally posing a comparative framework of minibinder 8.6 over HBD3, as a more potential adjuvant, apprehending wet-lab proof.

The functional role of HMGB3 in ESCC proliferation and metastasis was illustrated in our research. Targeting the TGIF2/HMGB3/TLR3/TGF-β axis has the potential to serve as a promising therapeutic approach.

Our finding that the antitumor activity of locally induced PF4 contrasts with its reported protumor effects when expressed systemically clarifies the context-dependent duality of PF4 in cancer. These results position TLR8 agonists as promising candidates for combination immunotherapy.

TLR3, TLR7, TLR8, and TLR9 are all expressed in OL-no, OL-dys, and OSCC. Also, the study provides evidence for possible nucleocytoplasmic shuttling of TLRs.

This study investigated the individual and combinatorial effects of TLR3 Poly(I:C), TLR5 (Flagellin), and TLR7 (Imiquimod) ligands on nitric oxide (NO) production and pro-inflammatory cytokine expression in RAW 264.7 mouse macrophage cells...These findings highlight a potent crosstalk between TRIF-dependent (TLR3) and MyD88-dependent (TLR7, TLR5) signaling pathways, leading to amplified immune activation. Our study highlights the potential of synergistic TLR ligand combinations as powerful immunomodulators, offering promising avenues for the rational design of more effective vaccine adjuvants and innovative strategies in cancer immunotherapy.

These findings not only support the pharmacological basis of using toad to treat inflammatory diseases in the Chinese medical history, but also provide a promising anti-inflammatory drug candidate for future clinical application.

Via RBRIII, MYC suppresses the accumulation of R-loop-derived RNA-DNA hybrids and prevents them from activating the innate immune kinase TBK1 via the TLR3 pattern recognition receptor. Our data demonstrate that the phase transition of MYC is an RNA-driven stress response that suppresses the accumulation of immunogenic RNA-DNA hybrids.

In addition, redundancy analysis revealed the correlations between enzyme activities and differentially expressed genes. Overall, these results demonstrate that V. harveyi infection compromises hepatic health in hybrid grouper by inducing structural damage to the liver, perturbing oxidative stress, and impairing both immune function and metabolic processes.

The observed discrepancies in LL-37 function across studies highlight its complex, context-dependent role in tumor biology. Further research is needed to elucidate the mechanistic basis of LL-37 signaling and its potential as a therapeutic target in CRC.

Structural characterization identified nine high-impact nsSNPs (ΔΔG <  - 1.7 kcal/mol), particularly in TLR3 (L104N, L381P, L77P) and CD274 (W57S, C155S, G159D, Y112N), indicating potential disruption of receptor stability, immune checkpoint interactions, and inflammasome regulation. This integrative multi-omics and structural pharmacogenomics framework reveals a robust four-gene signature (CASP1, TLR3, PYCARD, CD274) that links necroptosis, ferroptosis, and immune modulation in BRCA, providing promising avenues for precision oncology and therapeutic target development.

Sustained IFN-β secretion subsequently inhibits NSCLC cell proliferation and reprograms the tumor microenvironment by increasing the infiltration levels of CD4+ T cells, M1 macrophages and NK cells. Our findings revealed a reciprocal negative feedback loop in the regulation of IFN-β signaling, highlighting the role of the TRIM3/TLR3 axis in the suppression of NSCLC progression and offering a promising strategy to suppress tumor growth and enhance immunotherapy efficacy in NSCLC.

This study did not establish a clear prognostic role for TLR-3, TLR-4, or TLR-9 in oral cavity SCC. However, the findings highlight the biological complexity of TLR-mediated pathways in cancer. Further large-scale, multi-institutional studies are necessary to better understand the clinical relevance of TLRs in oral carcinogenesis.