The ability of effector T helper cells to switch from a pro- to an anti-inflammatory function, i.e. immune adaptation, is fundamental for intestinal homeostasis. We hypothesize that immune adaptation in the intestine is controlled by the availability of ATP and adenosine (ADO) in the intestinal environment. In this second period we will address (i) the consequences of ATP sensing by intestinal Th17 cells, (ii) the role of cell- and extracellular vesicle-associated purinergic enzymes in the ATP to ADO degradation in the intestine, (iii) the consequences of the loss of adenosine A2A receptor signaling in Th17 cells, and (iv) the molecular mechanisms regulating the expression of CD73 and A2A receptors in Th17 cells.
DFG Programme
Collaborative Research Centres
