CD8 (cluster of differentiation 8)

P1, N=15, Not yet recruiting, National Institute of Neurological Disorders and Stroke (NINDS)

In COAD, a subset of patients in stage II/III with CD3+RUNX3+high/CD8 + high may be spared adjuvant treatment due to excellent prognosis. However, further studies are needed to confirm and elucidate the protective role of CD3+RUNX3+ cells in COAD and LUAD.

Importantly, we demonstrated that AA synergized with anti-PD-L1 therapy while maintaining a favorable safety profile. This study identifies AA as a novel HDAC8 inhibitor that remodels the TME, offering a promising strategy to overcome immunotherapy resistance in HCC.

Following infusion, T cell responses are detected in tumor and blood of a patient, and display activated/exhausted and cytotoxic phenotypes. A first-in-human clinical trial (NCT04625205) recently further validated proof-of-concept, supporting continued development of this ACT approach.

Oral Lm-based cancer vaccines targeting CRC elicit robust, widely disseminated, and persistent tumor-specific immune responses in mice. These vaccines limit CRC development when administered prophylactically and provide tumor control when administered therapeutically with ICI. Thus, oral delivery of Lm-based cancer vaccines coupled with ICI may provide improved control of CRC progression in clinical application.

Furthermore, CCR6 inhibition potentiated the efficacy of anti-PD1 immune checkpoint blockade. Taken together, our data demonstrate that tumor cell-derived CCL20 shapes an immunosuppressive microenvironment in pancreatic cancer by recruiting CCR6+ Tregs, suggesting that targeting the CCL20-CCR6 axis offers a promising therapeutic strategy, particularly when combined with immune checkpoint blockade.

Importantly, blocking the PSA-CD56/Siglec-7 interaction with specific antibodies restored T cell effector functions and triggered apoptosis of ccRCC cells. Our study unveils the PSA-CD56/Siglec-7 axis as a novel glyco-immune checkpoint, which represents a promising target for therapeutic interventions in ccRCC.

Our study establishes a novel multi-gene diagnostic signature for oxaliplatin resistance through integrative bioinformatics and machine learning approaches. The comprehensive molecular characterization and identification of potential therapeutic candidates provide new insights into resistance mechanisms and clinical management strategies for oxaliplatin-resistant colorectal cancer.

A reduction in PVL was also observed in a subset of ex vivo PBMC cultures derived from individuals with HAM/TSP exhibiting high viral proliferative activity. These results suggest that DMF suppresses pathogenic immune activation in HAM/TSP and may therefore represent a promising therapeutic candidate for this disabling neuroinflammatory disorder.

In conclusions, FRA inhibited ESCC cell growth and immune evasion by inactivating HIF-1α/STAT3/PD-L1 signaling in vitro and vivo. This study suggested that FRA may serve as a potential therapeutic agent for ESCC treatment.

Finally, we find that induced systemic SIAH2 expression promotes CD8 T cell infiltration into subcutaneous tumors in a syngeneic mouse model. Our work further supports the tumor suppressive role of PLK3 in lung cancer and discovered a novel involvement of PLK3 in the regulation of the immune microenvironment of lung tumors.

As fasting alone failed to improve the symptoms, prednisolone (PSL) was initiated, resulting in amelioration of both symptoms and endoscopic findings. Cemiplimab-induced immune-related gastritis can be diagnosed based on its characteristic endoscopic and histopathological features, similar to irAE gastritis caused by other immune checkpoint inhibitors.