CD73: Friend or Foe in Lung Injury

Ecto-5 '-nucleotidase (CD73) plays a strategic role in calibrating the magnitude and chemical nature of purinergic signals that are delivered to immune cells. Its primary function is to convert extracellular ATP to adenosine in concert with ectonucleoside triphosphate diphosphohydrolase-1 (CD39) in normal tissues to limit an excessive immune response in many pathophysiological events, such as lung injury induced by a variety of contributing factors. Multiple lines of evidence suggest that the location of CD73, in proximity to adenosine receptor subtypes, indirectly determines its positive or negative effect in a variety of organs and tissues and that its action is affected by the transfer of nucleoside to subtype-specific adenosine receptors. Nonetheless, the bidirectional nature of CD73 as an emerging immune checkpoint in the pathogenesis of lung injury is still unknown. In this review, we explore the relationship between CD73 and the onset and progression of lung injury, highlighting the potential value of this molecule as a drug target for the treatment of pulmonary disease.

Automated summary

Ecto-5'-nucleotidase (CD73) plays a crucial role in regulating the intensity and nature of purinergic signals in immune cells. It converts extracellular ATP to adenosine along with CD39 to limit excessive immune responses. The location of CD73 near adenosine receptors determines its positive or negative effects, and its action is influenced by nucleoside transfer. However, the bidirectional nature of CD73 in lung injury pathogenesis is still unknown. This review explores the relationship between CD73 and lung injury, highlighting its potential as a drug target for pulmonary disease treatment.