The safety and strong antitumor effects of GPC1-specific CAR-T cells against GPC1-expressing solid tumors were demonstrated by using both syngeneic and xenogeneic mouse models.

Downregulation of mitochondrial activity by immunosuppressive tumor-derived soluble factors leads to systemic unresponsiveness to the PD-1 blockade therapy.

The interplay between the cytokine TGFβ and the PD-1/PD-L1 pathway promotes CD8+ T cell anergy and tolerance towards transplanted tissues.

SLAMF6 is an inhibitory checkpoint of T cells, the lack of which leads to better tumor control, suggesting a new immunotherapy target.

Cancer cell expression of the T-cell co-stimulatory molecule CD80, or treatment with agonistic antibodies targeting the T-cell co-stimulatory receptors OX-40 or 4-1BB, enhances the anti-tumor activity of FAK inhibition.

Immune checkpoint inhibition therapy for cancer paradoxically activates tuberculosis infection, and advanced human cell culture modelling demonstrates excess TNF-α section is the primary driver.

CD301b dendritic cells potently suppress antibody responses by limiting the activity of follicular helper T cells and germinal center B cells.

Tumor-infiltrating regulatory T cells are regulated by the immunoreceptor CD300a, which suppresses signals from tumor-derived extracellular vesicles.

Cluster analysis reveals convergent T cell clones reacting to tumor antigens, enabling intelligent optimization of cancer immunotherapy.

Tumor stiffness blocks T cell migration in tumors.