For example, in ovarian carcinoma animal models, CD11b+Gr-1+cells with a high expression of PD-L1 and CD80 markedly inhibited antigen-specific immune responses, whereas blockade of PD-L1 and CD80 in Gr-1+CD11b+cells abrogated immune suppression.84, 85 MDSCs derived from IL-10-stimulated DCs exhibited enhanced PD-L1 expression, and these cells induced T-cell dysfunction via the PD-L1/PD-1 signaling pathway.86 These results uncover the role of MDSCs in regulating T-cell exhaustion in cancer. This evidence concerns the gene CD274 and cancer.