Targeting the PD-1/B7-H1(PD-L1) Pathway to Activate Anti-Tumor Immunity

Curr Opin Immunol. 2012 Apr;24(2):207-12. doi: 10.1016/j.coi.2011.12.009. Epub 2012 Jan 9.

Abstract

Genetic alterations and epigenetic dysregulation in cancer cells create a vast array of neoepitopes potentially recognizable by the immune system. Immune checkpoint blockade has the capacity to enhance and sustain endogenous immunity against non-mutated tumor-associated antigens as well as uniquely mutant antigens, establishing durable tumor control. Recent evidence from preclinical models highlights the pivotal role of the Programmed Death-1 (PD-1) T cell co-receptor and its ligands, B7-H1/PD-L1 and B7-DC/PD-L2, in maintaining an immunosuppressive tumor microenvironment. Encouraging early clinical results using blocking agents against components of the PD-1 pathway have validated its importance as a target for cancer immunotherapy.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • B7-H1 Antigen / immunology
  • Humans
  • Ligands
  • Neoplasms / immunology*
  • Neoplasms / metabolism
  • Programmed Cell Death 1 Receptor / immunology
  • Signal Transduction*

Substances

  • B7-H1 Antigen
  • Ligands
  • Programmed Cell Death 1 Receptor