TLR5 (Toll Like Receptor 5)

These results underscore the importance of considering the tissue-resident microbiome as a biomarker of risk to improve primary prevention of breast cancer. Significance: Obesity differentially modulates non-cancerous breast tissue microbial-associated molecular pattern signaling, enriching LPS and flagellin, to promote oxidative stress and DNA damage.

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.

Novel hydrophilic multivalent linkers enable very high drug-to-antibody ratios and dual-payload ADCs, while modulation of MDAS, TLR7, TLR5, and STING pathways induces p16+ immune subsets that promote disease tolerance. Together, these inventions highlight convergent mechanisms for improving efficacy, resilience, and therapeutic durability.

Collectively, these data identify a role for P. aeruginosa in promoting bladder cancer progression through TLR5-ERK1/2-CCL20-mediated MDSC recruitment, shedding light on the intricate interplay between microbial infection and cancer pathogenesis. These insights highlight potential therapeutic targets to disrupt infection-driven cancer progression.

This research provides a computationally optimized vaccine design that shows potential for eliciting immune responses against H. pylori. Importantly, the findings remain entirely theoretical and require rigorous experimental validation in vitro and in vivo to assess their immunological relevance, safety, and efficacy before any translational or clinical application can be considered.

Acute pharmacologic blockade of TLR5 in tumor-bearing mice altered the composition of tumor-associated myeloid populations, reducing the frequency of monocytes and CCR2-expressing macrophages accumulating within the TME of WT mice. These data reveal that chronic TLR5 signaling, driven by tumor-induced loss of gut barrier integrity, promotes expansion of myeloid cells within the bone marrow and is a host-intrinsic mechanism driving accumulation of immature monocytes and macrophages into the TME.

Given the safety and T cell stimulation profiles of the chaperone-antigen complex vaccine already established in our recent clinical trial, this new generation of chaperone cargo, capable of delivering both antigenic targets and pathogen-associated immunoactivating signals simultaneously, represents a promising strategy to potentially improve the low response rates in patients receiving immune checkpoint inhibitors.

Our data suggest innate immune deficiencies may interact with previously described keratinocyte abnormalities, amplifying local immune dysfunction. These findings provide a framework for investigating TLR-based therapeutic approaches in EV.

This study generates further understanding toward the goal of developing a broad prophylactic strategy against HCV that is readily available and potentially amenable to future clinical use, offering hope in the fight against HCV. The online version contains supplementary material available at 10.1007/s40203-025-00448-9.

The current study demonstrates that PPARγ activation exerts anti-H. pylori effects during gastric ulcer progression by inhibiting the TLR/NF-κB signaling pathway.

The differing TLR expression patterns indicate diverse immune mechanisms involved in EV-related carcinogenesis, suggesting that TLRs could be potential therapeutic targets, meriting further investigation into their roles in tumour growth regulation.

We found that NK cells express TLR2 and TLR5, and that exposure to supernatants from ESKAPE group bacteria modified their cytotoxicity against JEG-3 and K-562 cell lines and their NKG2A and IL-10 mRNA levels. Our findings indicate that bacteria can modify NK cell features and their interactions with other cells in the microenvironment.