CD80 (CD80 Molecule)

Differences were identified between UPS and MFS in the composition of lymphoid cell populations and in the intercellular interactions. This proposes deeper understanding of the biological differences between these sarcoma subtypes and may be important for the development of new therapeutic approaches, although further validation of the findings is required.

Our study identified SIRT expression in macrophages of the DLBCL environment and specifically the importance of SIRT1 in the DLBCL M1 macrophage immune microenvironment. This opens an avenue for the potential translational exploitation of SIRT1 modulation as therapeutic target in this hematological malignancy.

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.

Our study provides no evidence that sICs can predict LNM in PeCa, although four inhibitory sICs were significantly elevated in PeCa patients compared to cancer-free controls, suggesting systemic immunosuppression associated with tumor presence, consistent with findings in other malignancies. Studies with larger cohorts are warranted to clarify the prognostic significance of sICs in PeCa.

Complement activation and the accumulation of M2-like macrophages are associated with anti-human MDA5 monoclonal antibody-induced hepatic injury in mice. These findings provide mechanistic insight into antibody-complement-macrophage interactions and suggest that modulation of complement pathways may represent a potential therapeutic approach to limit liver and systemic involvement in this disorder.

Despite the limitations of an in vitro PBMC-based system, selective VEGFR-1 blockade by D16F7 mAb alleviates VEGF-A-driven immune tolerance while preserving T-cell activation, supporting its translational potential as a complementary immunomodulatory approach.

In conclusion, our findings indicate that CL-387785 induces necroptosis in tumor cells via the TRADD/RIPK1/NF-κB/CD80 signaling pathway, thereby sensitizing tumors to anti-PD-1 therapy. These results suggest that CL-387785 is a promising candidate for increasing tumor immunotherapy efficacy.

Our study demonstrates that a CLDN18.2-targeting DC vaccine can effectively induce potent antigen-specific CTL responses and elicit significant antitumor immunity in a preclinical model. These findings provide a strong rationale for the clinical development of CLDN18.2-directed DC-based immunotherapy for gastric cancer.

Our data demonstrated that CD80 modulated tumor-cell stemness and malignant phenotype while restraining antitumor T cell immunity. Targeting CD80 augments antitumor immunity and provides a compelling strategy to enhance treatment responses to neoadjuvant chemoimmunotherapy in HNSCC.

Functional analysis revealed that the pathways enriched in glioma tissues with high SLAMF9 expression were associated with immune response-related pathways. This study is the first to highlight the important clinical value of SLAMF9 in patients with glioma.

These results demonstrate that an RT-based combination therapy that robustly induces CD4+ T cells alongside CD8+ T cells can elicit a strong abscopal response and suggest that CD4+ effector T cells act at abscopal sites by promoting DC-mediated cross-presentation of tumor antigens to CD8+ T cells originating from the irradiated tumor.

Intriguingly, transient CD28 blockade decreased levels of certain TME cytokines without significantly affecting survival of CAR T cell treated mice. Collectively, these data provide direct evidence that endogenous CD28 signaling modulates CAR T cell responses in multiple myeloma and lymphoma models.