CD69 (CD69 Molecule)

The Fc-optimized anti-CD276 antibody 8H8_SDIE effectively enhanced NK cell reactivity against CD276-positive CRC cells and induced tumor cell lysis in vitro. These findings suggest that 8H8_SDIE holds potential as a novel immunotherapeutic candidate for CRC, particularly for patients with microsatellite-stable disease, and warrants further evaluation in advanced preclinical and future clinical studies.

We identified a feasible method to activate CD56+ cells and evaluate the safety of their infusion in patients. Despite the value of activating CD56+ cells with IL-15, further studies with larger sample sizes are needed to confirm and validate the current hypothesi (registration number: IRCT20230801058996N2).

We successfully developed TIPE2-downregulated NKG2D-CAR-T cells that exhibited enhanced activation and cytotoxicity while limiting apoptosis and exhaustion against NKG2D ligand-expressing pancreatic tumors, highlighting TIPE2 as a promising intracellular immune checkpoint target for optimizing CAR-T cell therapy in solid tumors.

Although ex vivo expanded TILs are predominantly terminally differentiated, exhausted and transcriptionally highly distinct from the initial TILs, there is also a large progenitor exhausted CD8 T cell (Tpex) population and DN numbers increase. Future work to amplify subpopulations of TILs with memory cell phenotypes, such as the DN cells, will likely further improve this therapy.

ANXA2 drives HCC immune evasion by upregulating exosomal PD-L1 via CD63 stabilization, offering a novel target to enhance ICB efficacy. This work highlights a tumor-specific exosome regulation mechanism, with potential implications for immunotherapy across exosome-dependent cancers.

Results showed that EVs induced an increase in CD69 expression, cytotoxicity, and TNF-α and IFN-γ production in γδ T cells in a MIC-dependent mechanism. These results provide valuable insights for developing targeted immunotherapies in GBM patients.

Collectively, these findings demonstrate that VitD reprograms the immune response to PDT by enhancing cytotoxic immunity while limiting immunosuppressive features. This suggests an immune-priming strategy to consider, possibly alongside immune checkpoint blockade, for treating cutaneous SCC.

This study defines a core set of genes and TFs that critically regulate the initial activation of human naïve CD8+ T cells. These results provide a molecular roadmap for future efforts to engineer more potent and durable CD8+ T cell responses for adoptive cell therapy.

Furthermore, donors with higher baseline percentages of γδ T cells, CD19+ B cells, CD4 T cells, Vδ2 Naïve, Vδ2 TemRA, CD3+CD25+, and Vδ2+CD25+; and low Effector Memory CD3+ and Vδ1+ T cells were associated with fewer Cytomegalovirus (CMV) reactivation in their recipients. The present study underscores the importance of compositional analysis of immune cells in both recipients and donors as a discerning predictive tool for anticipating long-term clinical outcomes following allogeneic HSCT and highlights the need for future validation in larger cohorts.

To demonstrate the usefulness of the method for immunotherapy applications, we investigated the interaction of primary multiple myeloma cells with the therapeutic monoclonal antibodies daratumumab and isatuximab and a polyclonal anti-CD38 antibody. Our approach might lay the foundation for improved personalized diagnostics and treatment with therapeutic antibodies.

The functional phenotype and differentiation pattern of peripheral blood T lymphocytes exert a critical impact on the therapeutic response to this triple therapy. https://www.clinicaltrials.gov/study/, identifier NCT06208033.

Understanding how different expanded TIL subgroups impact treatment response helps to recognize new biomarkers and therapeutic targets. This review investigates functions of TIL populations beyond the traditional markers like CD3 and CD8 across different cancers while concentrating on predictive outcomes in immunotherapy.