Combination GITR targeting/PD-1 blockade with vaccination drives robust antigen-specific antitumor immunity

Oncotarget. 2017 Jun 13;8(24):39117-39130. doi: 10.18632/oncotarget.16605.

Abstract

Tumor progression is facilitated immunologically by mechanisms that include low antigen expression, an absence of coimmunostimulatory signals, and the presence of regulatory T cells (Tregs), all of which act to suppress and restrict effector T cells in the tumor. It may be possible to overcome these conditions by a combination of modulatory immunotherapy agents and tumor-antigen targeting to activate and drive effective antitumor T cell responses. Here, we demonstrated that co-administration of aGITR and aPD-1 monoclonal antibodies (mAb) in combination with a peptide vaccine (Vax) in mice bearing established tumors significantly delayed tumor growth and induced complete regression in 50% of the mice. This response was associated with increased expansion and functionality of potent Ag-specific polyfunctional CD8+ T cells, reduced Tregs, and the generation of memory T cells. Tumor regression correlated with the expansion of tumor-infiltrating antigen-specific CD8+ effector memory T cells, as depletion of this cell population significantly reduced the effectiveness of the triple combination Vax/aGITR/aPD-1 therapy. These findings support the concept that dual aGITR/aPD-1 combination with cancer vaccines may be a novel strategy against poorly immunogenic tumors.

Keywords: GITR; PD-1; immuno-oncology; immunotherapy; vaccines.

MeSH terms

  • Animals
  • Antibodies, Monoclonal / pharmacology*
  • Antigens, Neoplasm / immunology*
  • Apoptosis
  • CD8-Positive T-Lymphocytes / immunology
  • Cancer Vaccines / administration & dosage*
  • Cell Proliferation
  • Female
  • Glucocorticoid-Induced TNFR-Related Protein / antagonists & inhibitors*
  • Immunotherapy
  • Melanoma, Experimental / immunology*
  • Melanoma, Experimental / metabolism
  • Melanoma, Experimental / therapy
  • Mice
  • Mice, Inbred C57BL
  • Programmed Cell Death 1 Receptor / antagonists & inhibitors*
  • T-Lymphocytes, Regulatory / immunology*
  • Tumor Cells, Cultured
  • Vaccination

Substances

  • Antibodies, Monoclonal
  • Antigens, Neoplasm
  • Cancer Vaccines
  • Glucocorticoid-Induced TNFR-Related Protein
  • Pdcd1 protein, mouse
  • Programmed Cell Death 1 Receptor
  • Tnfrsf18 protein, mouse