Figure 1.

The immune effects of adenosine axis in TME. (A) The eATP can be released in large quantities during cell necrosis, apoptosis and mechanical damage, and can be actively secreted by tumor cells and other cells in the TME, which is triggered by hypoxia, chronic inflammation, nutrient deprivation, or cytotoxic drugs. Extracellular ATP is broken down by CD39 to AMP, then CD73 to adenosine. Extracellular adenosine binds to A2AR on immunocytes such as T cells, NK cells and DC cells, inhibiting their immune function. (B) Role of monoclonal antibodies in adenosine axis. CD39 mAb prevents eATP from binding to CD39 to reduce AMP production; CD73 mAb prevents AMP from binding to CD73 to reduce ADO production. A2AR mAb prevents ADO from binding to A2AR and inhibits its immunosuppressive effect.