TLR2 (Toll Like Receptor 2)

Mechanistically, SMU-C409 activates TLR1/2, recruits MyD88, induces NF-κB phosphorylation, and stimulates TNF-α/IL-1β secretion; in vitro studies confirm robust immune cell activation and antitumor immunomodulation. SMU-C409 overcomes core limitations of TLR2 agonists while maintaining high potency, positioning it as a promising candidate for advancing cancer immunotherapy.

P. gingivalis products induce neuroinflammatory responses and Alzheimer's-like pathology in mouse models, supporting their role as contributors to neurodegeneration and potential targets for preventive strategies.

We discuss the contribution of all these molecules in major hallmarks of OSA-(1) proliferative and survival advantages, (2) metastasis and angiogenesis, and (3) immune evasion-and examine potential strategies for their combined targeting. By leveraging knowledge gained from other cancer models and integrating it with the distinct biological and clinical features of OSA, this perspective seeks to outline rational and innovative combinatorial strategies that may overcome current therapeutic limitations and ultimately improve patient outcomes.

These mechanisms mirror the molecular signature of inflammaging, supporting TLRs as actionable targets for restoring immune balance. Collectively, the evidence positions natural TLR modulators as a promising, yet untapped, avenue for promoting healthy aging and extending healthspan.

Finally, in silico cloning validated the vaccine's potential for efficient E. coli expression. These computational findings support the construct as a promising vaccine candidate against C. parvum and S. mansoni, warranting further experimental validation.

In conclusion, our study demonstrated that EVs containing HSP90α, derived from lenvatinib-resistant liver cancer cells, can promote EMT and drug resistance in HCC cells by stimulating CXCL8 secretion from macrophages. This finding may provide new insights and strategies to overcome lenvatinib resistance in the future.

Upon doxycycline withdrawal at 8 weeks of age, mice developed progressive cerebellar ataxia by 26 weeks and succumbed by 30 weeks...Prophylactic administration of the CSF1R inhibitor BLZ945 exacerbated motor deficits and demyelination, significantly increasing this microglial population. Similarly, MSR1+ and CD68+ microglia/macrophages were observed in early pontocerebellar lesions of six human MSA-C autopsy cases. These findings suggest that this pro-inflammatory microglia subset plays a central role in disease progression and may represent a promising therapeutic target for modifying the course of MSA-C and related synucleinopathies.

This study provides a reliable prognostic tool for lung cancer and offers insights into the critical role of the immune microenvironment in lung cancer pathogenesis. Our findings may guide the development of personalised immunotherapy strategies for lung cancer patients.

When applied as a prophylactic cancer vaccine, they not only delayed tumour growth but also reshaped the antitumour immune landscape, characterized by enhanced CTL responses, reduced regulatory T cell frequencies and diminished exhausted CD8⁺ T cell populations. Collectively, these findings highlight the potential of I-PDNVs as dual-function PDNVs, serving both as immunotherapeutic agents and as vaccine delivery platforms for applications requiring reinforced Th1, CTL and NK cell responses.

This study revealed the critical role of the NETs-STC1 feedback loop in BLCA immunoresistance. Targeting this axis could simultaneously enhance efficacy and safety of immunotherapy, providing a novel translational strategy for overcoming resistance in clinical settings.

Heat shock protein 60 (HSP60) was identified as the key molecule on LC3+ EVs that induced the reduction of occludin and ZO-1 through the Toll-like receptor 2 (TLR2)-myeloid differentiation primary response protein MyD88 (MYD88)-Snail Family Transcriptional Repressor 1 (Snai1) signal cascade. Combined with our previous findings, these results demonstrate that removing circulating LC3+ EVs or targeting HSP60 on LC3+ EVs might be a promising way to prevent breast cancer lung metastasis.

Our study revealed that several TLR2 ligands, each with different specificities, elicited diverse responses in primary cortical cells. In conclusion, TLR1-TLR2 and TLR2-TLR6 signaling reduces the peak amplitude and induces cell death, and TLR1-TLR2 signaling enhances Ca2 + dynamics via a TNFα pathway.