Targetting the PD-L1/PD-1 axis holds promise in the treatment of malignancy

Tumor cells create an immunologic milieu characterized by the disruption of effective antigen presentation, loss of effector cell function and complexity, and upregulation of pathways that promote tolerance and T cell anergy (1,2). A critical element of tumor mediated immunosuppression is the presence of the negative checkpoint molecules CTLA-4 and PDL-1/PD-1 that inhibit immune activation and the expansion of antigen specific T cells (3).