Sheng Yao

TL;DR: It is suggested that oncogenic activation of the AKT-mTOR pathway promotes immune escape by driving expression of PD-L1, which was confirmed in syngeneic and genetically engineered mouse models of lung cancer where an mTOR inhibitor combined with a PD-1 antibody decreased tumor growth, increased tumor-infiltrating T cells, and decreased regulatory T cells.

TL;DR: These data represent the most prolonged observation to date of patients with solid tumors responding to anti- PD-1 immunotherapy and the first report of successful reinduction therapy following delayed tumor progression, and underscore the potential for immune checkpoint blockade with anti-PD-1 to reset the equilibrium between tumor and the host immune system.

TL;DR: It is reported that B7-H1 on cancer cells receives a signal from PD-1 to rapidly induce resistance against T cell-mediated killing, a new mechanism by which cancer cells use a receptor on immune cells as a ligand to induce resistance to therapy.

TL;DR: It is found that PD-L1 is weakly expressed at a low frequency in untreated human and murine PDAs but treatment with a granulocyte macrophage colony-stimulating factor secreting PDA vaccine (GVAX) significantly upregulates PD- L1 membranous expression after treatment of tumor-bearing mice, and combination therapy with vaccine and PD-1 antibody blockade improved murine survival.

TL;DR: It is demonstrated that the B7-H1/CD80 pathway is a crucial regulator in the induction and maintenance of T-cell tolerance.