Co-inhibition of CD73 and A2AR Adenosine Signaling Improves Anti-tumor Immune Responses

Cancer Cell. 2016 Sep 12;30(3):391-403. doi: 10.1016/j.ccell.2016.06.025.

Abstract

Preclinical studies targeting the adenosinergic pathway have gained much attention for their clinical potential in overcoming tumor-induced immunosuppression. Here, we have identified that co-blockade of the ectonucleotidase that generates adenosine CD73 and the A2A adenosine receptor (A2AR) that mediates adenosine signaling in leuokocytes, by using compound gene-targeted mice or therapeutics that target these molecules, limits tumor initiation, growth, and metastasis. This tumor control requires effector lymphocytes and interferon-γ, while antibodies targeting CD73 promote an optimal therapeutic response in vivo when engaging activating Fc receptors. In a two-way mixed leukocyte reaction using a fully human anti-CD73, we demonstrated that Fc receptor binding augmented the production of proinflammatory cytokines.

Keywords: CD73; adenosine; combination therapy; immunotherapy; tumor.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 5'-Nucleotidase / antagonists & inhibitors*
  • 5'-Nucleotidase / immunology
  • Adenosine A2 Receptor Antagonists / pharmacology*
  • Animals
  • Antibodies, Monoclonal / immunology
  • Antibodies, Monoclonal / pharmacology
  • Female
  • Humans
  • Immune Tolerance / immunology*
  • Male
  • Mammary Neoplasms, Experimental / immunology
  • Mammary Neoplasms, Experimental / therapy
  • Melanoma, Experimental / immunology
  • Melanoma, Experimental / therapy
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Neoplasms / immunology*
  • Neoplasms / pathology
  • Neoplasms / therapy*
  • Receptor, Adenosine A2A / immunology
  • Signal Transduction

Substances

  • Adenosine A2 Receptor Antagonists
  • Antibodies, Monoclonal
  • Receptor, Adenosine A2A
  • 5'-Nucleotidase