Extracellular adenosine triphosphate (eATP) mediates pro-inflammatory
responses by recruiting and activating inflammatory cells. eATP is
hydrolyzed by CD39 to adenosine monophosphate (AMP), which is converted
to the immunosuppressive nucleoside adenosine (ADO) by CD73. CD39 is the
rate-limiting enzyme in this cascade and can be viewed as an
immunological switch that shifts ATP-driven pro-inflammatory immune cell
activity to an anti-inflammatory state mediated by ADO. CD39 is
expressed by a broad range of immune cells and can be influenced by
genetic and environmental factors. Accumulating evidence suggests that
CD39 is involved in several pathophysiological events, such as
inflammatory bowel diseases, sepsis, ischemia-reperfusion injury,
allergic diseases, systemic lupus erythematosus, diabetes, and cancer.
Here, we focus on the current understanding of CD39 in immunity, and
presents a comprehensive picture of the multiple roles of CD39 in a
variety of disorders.