PDL1 Signals through Conserved Sequence Motifs to Overcome Interferon-Mediated Cytotoxicity

Cell Rep. 2017 Aug 22;20(8):1818-1829. doi: 10.1016/j.celrep.2017.07.075.

Abstract

PDL1 blockade produces remarkable clinical responses, thought to occur by T cell reactivation through prevention of PDL1-PD1 T cell inhibitory interactions. Here, we find that PDL1 cell-intrinsic signaling protects cancer cells from interferon (IFN) cytotoxicity and accelerates tumor progression. PDL1 inhibited IFN signal transduction through a conserved class of sequence motifs that mediate crosstalk with IFN signaling. Abrogation of PDL1 expression or antibody-mediated PDL1 blockade strongly sensitized cancer cells to IFN cytotoxicity through a STAT3/caspase-7-dependent pathway. Moreover, somatic mutations found in human carcinomas within these PDL1 sequence motifs disrupted motif regulation, resulting in PDL1 molecules with enhanced protective activities from type I and type II IFN cytotoxicity. Overall, our results reveal a mode of action of PDL1 in cancer cells as a first line of defense against IFN cytotoxicity.

Keywords: B7-H1; CD274; PD-L1; PD1; PDL1; immunotherapy; interferon; signal transduction.

MeSH terms

  • Animals
  • B7-H1 Antigen / immunology*
  • Cell Line, Tumor
  • Female
  • HEK293 Cells
  • Humans
  • Interferons / immunology*
  • Mice
  • Mice, Inbred C57BL
  • Neoplasms / immunology*
  • Signal Transduction

Substances

  • B7-H1 Antigen
  • CD274 protein, human
  • Cd274 protein, mouse
  • Interferons