Proposed model of leukocyte-endothelial cross-talk at sites of inflammation. In areas of ongoing inflammation, diminished oxygen supply coordinates the induction of CD39 and CD73. At such sites, activated PMNs provide a readily available extracellular source of ATP, which through 2 enzymatic steps is metabolized to adenosine. Adenosine generated in this fashion is available for activation of PMN adenosine receptors, particularly the AdoRA_2A and AdoRA_2B, leading to decreased in PMN adhesion and transmigration. As such, this form of leukocyte-endothelial cell cross-talk may provide an innate mechanism to dampen ongoing inflammatory responses.