Constitutive and acquired mechanisms of resistance to immune checkpoint blockade in human cancer

Cytokine Growth Factor Rev. 2017 Aug:36:17-24. doi: 10.1016/j.cytogfr.2017.06.002. Epub 2017 Jun 2.

Abstract

Cancer immunotherapy with monoclonal antibodies directed against regulatory pathways in T lymphocytes has been revolutionizing medical oncology, and the clinical success of monoclonal antibodies targeting either cytotoxic T lymphocyte antigen-4 (CTLA-4) or program death-1 (PD-1) in patients affected by melanoma, Hodgkin's lymphoma, Merkel cell carcinoma, and head and neck, bladder, renal cell or non-small cell lung cancer is way beyond the most optimistic expectation. However, immune checkpoint blockade (ICB) has failed to arrest progression in a consistent amount of patients affected by those tumors, and various histological types, including breast, colon and prostate cancer, are less sensitive to this therapeutic approach. Such clinical findings have fueled massive research efforts in the attempt to identify pre-existing and acquired mechanisms of resistance to ICB. Here we focus on evidences emerging from studies in humans on how tumor cells and the tumor microenvironment contribute to the heterogeneous clinical responses, and we propose strategies stemming from pre-clinical models that might improve clinical outcomes for patients.

Keywords: Cancer immunotherapy; Immune checkpoint; Interferon; Monoclonal antibodies; Resistance; T lymphocytes.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / therapeutic use*
  • CTLA-4 Antigen / immunology
  • Carcinoma, Non-Small-Cell Lung / immunology
  • Carcinoma, Non-Small-Cell Lung / therapy
  • Combined Modality Therapy
  • Drug Resistance, Neoplasm*
  • Humans
  • Immunotherapy*
  • Lung Neoplasms / immunology
  • Lung Neoplasms / therapy
  • Melanoma / therapy
  • Mice
  • Neoplasms / immunology
  • Neoplasms / therapy*
  • Programmed Cell Death 1 Receptor / immunology
  • T-Lymphocytes / immunology
  • Tumor Microenvironment*

Substances

  • Antibodies, Monoclonal
  • CTLA-4 Antigen
  • CTLA4 protein, human
  • Programmed Cell Death 1 Receptor