TLR8 (Toll Like Receptor 8)

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.

Five potential diagnostic biomarkers for AS-MCL1, F13A1, RGS2, TLR8, and TAGAP-were identified. In addition, the m5C regulator NSUN3 plays a critical role in macrophage function, providing experimental evidence that may support the diagnosis and treatment of AS.

Additionally, compared with the vector + M1 group, the TLR8 + M1 group exhibited up-regulated expressions of TLR8, MyD88, and TRAF6 proteins in macrophages, which could be reversed by EPH intervention. EPH can improve joint damage in RA rats, inhibit M1 macrophage polarization, and reduce the expressions of TLR8, MyD88, and TRAF6 proteins in cartilage tissue.

The results of analysis viral genes mRNA expression suggested potential role of viral genes during BKV pathogenesis. The results of this limited study showed that at the mRNA level, certain genes of the immune system can be altered and that BKV reactivation has the potential to affect these genes.

Extracellular delivery of miR-132-5p and miR-9-5p to co-cultures of iNeurons and iMGLs resulted in reduced neurite length. Our data establish that distinct CNS disease-associated miRNAs serve as signaling molecules for human microglia via TLR8, thereby controlling the diverse microglial functions and modulating the neuroinflammatory response.

In summary, endosomal TLRa VLPs all have the ability to activate pDCs, however, combined TLR7/8 activation using TLR7/8a VLPs was significantly more effective than the other VLPs at activating T cells and was dependent on direct contact with pDCs. Therefore, TLR7/8a VLPs may potentially induce a robust anti-tumor immune response and warrant further investigation for cancer therapy.

Notably, the most potent compound 69 significantly suppressed tumor growth in vivo in the CT26 mouse tumor model after intratumoral administration. These results highlight the potential of quinazolinone-based compounds as promising candidates for further development of new immunomodulatory agents targeting TLR7 and TLR8.

Ultimately, it was determined that all three genes were associated with the 'chemokine signalling pathway'. The prognostic signature comprised of MPO, CCL3, and TLR8 based on NETs was established, which provided theoretical basis and reference value for the research of AML.

Elisa 8-OHdG and caspase-3 levels were not statistically significant. Compared to the control group, no statistically significant changes were observed in TLR1, TLR2, TLR3, TLR4, TLR6, TLR7, TLR8, and TLR9 gene expressions in the treatment group treated with 26.59 µM TQ for 48 h. TQ shows potential as an anticancer agent and may contribute to the development of therapeutic approaches for lung cancers.

We developed a CD47-mimetic self-peptide-modified liposomal system that targets SIRPα on Kupffer cells and delivers the TLR8 agonist ZG0895, currently in clinical trials in the U.S. and China...Importantly, this phagocytosis inhibition establishes a spatiotemporal window that facilitates co-delivery of doxorubicin (DOX) liposomes to HCC cells via GLUT1-mediated targeting, resulting in synergistic immunochemotherapeutic effects. This dual modulation strategy improves targeting precision, treatment durability, and therapeutic synergy, offering a unique intrahepatic approach that addresses key challenges in HCC management and accelerates the clinical translation of TLR8 agonist-based nanomedicines.

Novel approaches such as nanoparticle systems and endogenous RNA mimetics promise targeted modulation of TLR activity. Together, these developments emphasize the therapeutic potential of precision TLR modulation in immunologically complex diseases.