Objective

Blockade of PD-1-PDL-1 interactions holds great promise as a therapeutic strategy for triggering durable responses against tumour cells. Here we have studied the activation of human T cells in a range of cellular contexts. We observe that in the majority of donors, PD-1 blockade is capable of causing increases in IFNg production in response to stimulation with allogeneic dendritic cells, a viral peptide and chronically activated T cells. This increase in IFNg production was mirrored by increases in the secretion of potentially immuno-regulatory IL-10. Importantly these effects were also mirrored in cells isolated from both colon and lung tumours where we again observed increases IFNg and IL-10 production following PD-1 blockade. These results continue to highlight the important role of PD-1 in regulating T cell activation under a range of stimulation conditions.