title: Targeting the PD-1/B7-H1(PD-L1) pathway to activate anti-tumor immunity.
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.
authors.affiliation: Department of Surgery, Johns Hopkins University School of Medicine and Sidney Kimmel Comprehensive Cancer Center, Baltimore, MD 21287, USA. stopali1@jhmi.edu
authors.forename: Suzanne L
authors.initials: SL
authors.lastname: Topalian
authors.forename: Charles G
authors.initials: CG
authors.lastname: Drake
authors.forename: Drew M
authors.initials: DM
authors.lastname: Pardoll
mesh_terms: D000818:Animals; D060890:B7-H1 Antigen / Q000276:immunology; D006801:Humans; D008024:Ligands; D009369:Neoplasms / Q000276:immunology* / Q000378:metabolism; D061026:Programmed Cell Death 1 Receptor / Q000276:immunology; D015398:Signal Transduction
chemical_list: D060890:B7-H1 Antigen; D008024:Ligands; D061026:Programmed Cell Death 1 Receptor