Purinergic signaling has been recognized to play an important role in inflammation, angiogenesis, malignancy, diabetes and neural transmission. Activation of signaling pathways downstream of purinergic receptors may also be implicated in transplantation and related vascular injury. Following transplantation, the pro-inflammatory "danger signal" adenosine triphosphate (ATP) is released from damaged cells and promotes proliferation and activation of a variety of immune cells. Targeting purinergic signaling pathways may promote immunosuppression and ameliorate inflammation. Under pathophysiological conditions, nucleotide-scavenging ectonucleotidases, CD39 and CD73, hydrolyze ATP, ultimately to the anti-inflammatory mediator adenosine. Adenosine suppresses pro-inflammatory cytokine production and is associated with improved graft survival and decreased severity of graft-versus-host disease. Furthermore, purinergic signaling is both directly and indirectly involved in the mechanism of action of several existing immunosuppressive drugs, such as calcineurin inhibitors and mTOR inhibitors. Targeting of purinergic receptor pathways, in particular in the setting of combination therapies, could become a valuable immunosuppressive strategy in transplantation. This review article focuses on the role of the purinergic signaling pathway in transplantation, immunosuppression, and explores possible future applications in clinical practice. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.

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