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The interaction of B7H1 in tumor cells with programmed death-1 (PD-1) inT cells plays an important role in the suppression of immune responses. However,the effects of the expression of B7H1 and the PD-1/programmed death 1 ligand 1(PD-L1) complex on tumor cells themselves remain largely unknown. In order toclarify this, we induced apoptosis in a number of human pancreatic cancer cellswith different expression levels of B7H1 and designed small peptides to interferewith the function of B7H1. In this study, we chose 2 human pancreatic cancer celllines (BxPC-3 and Panc-1 cells). Cells with a high expression of B7H1 (BxPC-3cells and Panc-1 cells treated with interferon-γ) presented much lower levelsof drug-induced apoptosis after they were incubated with PD-1 immunoglobulin.Furthermore, the percentage of BxPC-3 apoptotic cells transfected with B7H1 siRNAwas higher compared to that of cells transfected with control siRNA. Both of theseresults indicate that the PD-1/PD-L1 complex transfers a reverse signal to B7H1+pancreatic cancer cells upon drug-induced apoptosis in vitro. This effect maybe a substantial factor for drug resistance during antitumor therapies. However,synthetic small peptides designed according to the amino acid residues of thePD-1/PD-L1 complex interrupt this effect successfully by their binding to cellmembranes and acting like a blocking agent. This result may lead to a breakthroughin pancreatic cancer treatment.

Synthetic small peptides acting on B7H1 enhance apoptosis in pancreatic cancer cells