TLR9 (Toll Like Receptor 9)

The formulation comprises a nanoplex (NP) encapsulating CpG ODN 1826 (CpG NP), which stimulates TLR-9 and elevates the levels of CD80/86 costimulatory molecules on antigen-presenting cells, and a NP incorporating CTLA-4 siRNA (siCTLA-4 NP), which suppresses the production of the immunological checkpoint molecule CTLA-4 on T cells...Ex-vivo study of cell composition in spleens and tumors, along with tumor-specific antigen stimulation assays on splenocytes, suggests that NC treatment can switch the immunosuppressive tumor microenvironment into an immunocompetent state. These findings demonstrate that our NC formulation, which integrates CTLA-4 suppression with DC stimulation, potentiates immune responses against tumor tissues, providing novel insights and potential applications in the field of cancer 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.

We confirmed separate lots of the 9vHPV vaccine contained low copy numbers of L1 DNA, but found 9vHPV vaccine-generated antibody responses were not dependent on DNA sensing. This study has thus refined our understanding of potential mechanisms underlying the strong and long-lasting antibody responses to HPV vaccination.

Complementary transcriptomic analysis using a compact four-gene Tα1 Response Index (Tα1-RI: TLR9, TLR2, IRF1, NLRC5) in TCGA-BRCA (n = 1,112) confirmed positive correlations with antigen presentation and cytotoxic programs and enrichment in CD8-like T cells in single-cell datasets. Collectively, these findings demonstrate that Tα1 enhances CD8+ T cell cytotoxicity while alleviating exhaustion, supporting its potential as an adjunct immunomodulator for improving immune surveillance in breast cancer.

The present review focuses on the relationship between mitochondria and T‑cell antitumor immune responses, exploring the core role of mitochondria in T‑cell tumor immunity from multiple aspects, including mitochondrial energy metabolism, mitochondrial dynamics and mitochondrial DNA. In addition, the present review examines state‑of‑the‑art research on antitumor therapies targeting mitochondria from multiple perspectives, with the aim of providing a reference for developing mitochondria‑targeted antitumor immunotherapy strategies.

The results of preclinical and early-stage clinical research indicate the potential application of tank-binding kinase 1 (TBK-1), fecal microbiota transplant (FMT), Toll-like Receptor 9 (TLR9), lipid nanoparticles (LNPs) containing a stimulator of an interferon gene agonist (STING), BRAF inhibitors, Lymphocyte Activation Gene (LAG-3), T-Cell Immunoglobulin and ITIM Domain (TIGIT), and oncolytic viruses (OVs) as potential methods to enhance melanoma sensitivity to ICB. To optimize immunotherapy, further research is needed to determine the detailed mechanisms of action, safety profiles, tolerability, and precise patient selection criteria for methods capable of overcoming melanoma's immunoresistance.

This review first summarizes the established knowledge on mitochondrial dysfunction in AKI, with emphasis on distinct mechanistic pathways activated by chemotherapy and immunotherapy. It then discusses emerging mitochondrial-targeted therapeutic strategies, logically integrating preclinical insights with data from ongoing and proposed clinical trials to present a coherent translational outlook.

This altered actin state led to an increase in BCR microcluster formation, amplification of NF-κB signaling, and resistance to inhibitors targeting chronic active BCR signaling. Hence, our study establishes RHOA and its mutant isoforms as critical regulators of oncogenic BCR signaling in DLBCL.

Further, high resolution SERS maps provided a spatial context of CD8 and VEGFR2 distribution that showed the molecular makeup of tumors in responder and nonresponder mice. Biomarker distribution in ex vivo SERS aligned with in vivo findings and showed moderate to strong correlations via a Pearson's correlation to quantification of IF markers in tumors.

Notably, therapeutic intervention using ODN2216-siPLD3 in murine models enhanced CD8 T cell infiltration and significantly inhibited tumor growth. Our findings highlight PLD3-high macrophages as a promising diagnostic biomarker and a therapeutic target for ESCC, paving the way for potential clinical translation.

Its context-dependent effects contribute to inconsistent clinical outcomes and raise concerns about safety and toxicity. This review examines the immunologic function and signaling mechanisms of TLR9, with a focus on its complex, context-specific, and "double-dealing" roles in cancer pathogenesis and therapy.

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.