Table 1.

Purinergic signaling and ectonucleotidases in inflammatory diseases.

Disease context	Mechanism	Reference
Airway inflammation	ATP triggers airway inflammation via P2X7 expression on dendritic cells	(11, 12)
Airway inflammation	P2Y6 receptor expressed on lung epithelial cells mediates IL-6 and IL-8 secretion upon allergen challenge	(13)
Airway inflammation	ATP activation of the P2Y2 receptor contributes to eosinophilic lung inflammation	(44, 45)
Cardiovascular disease	P2Y12 receptor deficiency reduces monocyte infiltration and plaque lesion area	(3)
Cardiovascular disease	Lack of the P2Y1 receptor decreases leukocyte infiltration into atherosclerotic plaques	(4)
Cardiovascular disease	Neointima injury results in upregulation of the P2Y2 receptor in rats, which in turn promotes leukocyte adhesion	(6, 7)
GvHD	ATP released from damaged cells aggravates GvHD by activation of antigen-presenting cells	(23, 73)
GvHD	P2Y2 deficiency in monocytes reduces GvHD severity by abrogating ERK activation and ROS production	(50)
GvHD	CD73 deficiency increases T cell allo-reactivity and aggravates murine GvHD	(65, 66)
Inflammatory bowel disease	CD39 deletion aggravates chemically induced colitis in mice	(57, 60)
	CD39 expression on Tregs is associated with better therapy response in inflammatory bowel disease patients
Inflammatory bowel disease	Lack of CD73 aggravates experimental inflammatory bowel disease in mice	(64)
Ischemia–reperfusion injury	CD39 plays a protective role by reducing vascular leakage	(56)
Lupus-associated nephritis	Inhibition of the P2X7 receptor reduces nephritis severity	(17)
Multiple sclerosis	ATP increases oligodendrocyte excitotoxicity and plaque formation via binding the P2X7 receptor	(15, 16)
	Gain of function polymorphisms of the P2X7 receptor are associated with increased MS risk
Platelet aggregation	Inhibition of P2Y12 signaling blocks platelet aggregation	(10)