Figure 11.

Bortezomib-mediated miR-155 and NF-κB signaling crosstalk to increase CD8⁺ T cell effector function. Bortezomib enhances crosstalk between the miR-155–SOCS1/SHIP1–T-bet–PD-1 axis and NF-κB signaling in CD8⁺ T cells. Bortezomib treatment increases NF-κB activity and miR-155 expression, thereby causing a decrease in its inhibitory targets SHIP1 and SOCS1. The inhibition of these targets in turn lead to decreased PD-1-mediated exhaustion and increased expression of effector molecules in CD8⁺ T cells.