TLR2 (Toll Like Receptor 2)

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.

This study demonstrated that the modified and more stable TLR2 agonist SUP3 provided an optimal strategy for promoting antitumor immunity via activation of cDC1. SUP3 enhanced antigen cross-presentation by cDC1 and subsequent activation of CTLs. The antitumor effect was further enhanced when SUP3 and Flt3L synergized with PD-L1 blockade. Therefore, reactivation of suppressed DCs in tumor microenvironment would be a promising strategy for designing effective antitumor immunotherapy.

Immune simulations predicted the strong cellular and humoral immune responses. These findings suggest that the designed vaccine holds substantial promise as a candidate for TNBC immunotherapy and merits further experimental validation.

Finally, codon optimization for Escherichia coli K12 using JCat yielded a guanine-cytosine content of 50.69% and a Codon Adaptation Index of 0.97, and in silico cloning into pET28a(+) using SnapGene confirmed high expression potential. Our results indicate that the designed vaccine is a viable candidate for both preventive and therapeutic measures against high-risk HPV, requiring additional laboratory and animal studies.

Different LCS criteria yield populations with highly varied characteristics. Risk-based criteria may provide more equitable eligibility across age groups.

Fracture models were established in Sprague-Dawley (SD) rats and intervened with the TLR-2 inhibitor C29 or the TLR-4 inhibitor TAK-242...These time-dependent effects significantly accelerated late-phase (>14d) fracture repair versus early stages (0-14d), improving bone healing parameters. Targeting TLR-2/4 accelerates fracture repair by suppressing MyD88/NF-κB-driven inflammation and optimizing the bone healing microenvironment.

This study investigated the pharmacodynamics and mechanism of SBPD in treating respiratory inflammation. SBPD protected mice against LPS-induced ALI by alleviating lung tissue damage. Through integrated investigation of the complete formulation and the monomer baicalin, it was collaboratively demonstrated that SBPD exerts anti-inflammatory effects via the NLRP3 inflammasome pathway.