Purinergic signaling and immune modulation at the schistosome surface?

After tissue stress or injury, intracellular ATP can be released into the extracellular environment. This signals cell damage because extracellular ATP acts as a danger-associated molecular pattern (DAMP) that is potently proinflammatory. Vertebrates temper this effect by catabolizing ATP to adenosine - a strongly anti-inflammatory molecule - using a set of characterized ectoenzymes (notably alkaline phosphatase, phosphodiesterase and ATP diphosphohydrolase). Strikingly, schistosomes in the bloodstream have this same set of ATP-catabolizing enzymes on their tegumental surfaces. It is our opinion that these function to remove the DAMP (ATP) released by host cells in response to schistosome intravascular migration. We propose this as one mechanism by which schistosomes prevent their hosts from focusing immunological mediators in their vicinity.