We have developed a cancer vaccine in which autologous tumor is fused with 
dendritic cells (DCs) resulting in the presentation of tumor antigens in the 
context of DC-mediated costimulation. In clinical trials, immunologic responses 
have been observed, however responses may be muted by inhibitory pathways. The 
PD1/PDL1 pathway is an important element contributing to tumor-mediated immune 
suppression. In this study, we demonstrate that myeloma cells and DC/tumor 
fusions strongly express PD-L1. Compared with a control population of normal 
volunteers, increased PD-1 expression was observed on T cells isolated from 
patients with myeloma. It is interesting to note that after autologous 
transplantation, T-cell expression of PD-1 returned to levels seen in normal 
controls. We examined the effect of PD-1 blockade on T-cell response to DC/tumor 
fusions ex vivo. Presence of CT-011, an anti-PD1 antibody, promoted the 
vaccine-induced T-cell polarization towards an activated phenotype expressing 
Th1 compared with Th2 cytokines. A concomitant decrease in regulatory T cells 
and enhanced killing in a cytotoxicity assay was observed. In summary, we 
demonstrate that PD-1 expression is increased in T cells of patients with active 
myeloma, and that CT-011 enhances activated T-cell responses after DC/tumor 
fusion stimulation.