Cekic, C.Linden, J.2018-04-122018-04-1220161474-1733http://hdl.handle.net/11693/38167Cellular stress or apoptosis triggers the release of ATP, ADP and other nucleotides into the extracellular space. Extracellular nucleotides function as autocrine and paracrine signalling molecules by activating cell-surface P2 purinergic receptors that elicit pro-inflammatory immune responses. Over time, extracellular nucleotides are metabolized to adenosine, leading to reduced P2 signalling and increased signalling through anti-inflammatory adenosine (P1 purinergic) receptors. Here, we review how local purinergic signalling changes over time during tissue responses to injury or disease, and we discuss the potential of targeting purinergic signalling pathways for the immunotherapeutic treatment of ischaemia, organ transplantation, autoimmunity or cancer.EnglishAdenosineAdenosine A2 receptorAdenosine A2b receptorAdenosine diphosphateAdenosine triphosphateNucleotidePurinergic P2 receptorPurinergic P2X receptorPurinergic P2Y receptorPurine derivativeAutoimmunityEffector cellExtracellular spaceGraft rejectionHeart muscle ischemiaImmune systemImmunocompetent cellImmunotherapyKidney ischemiaMacrophageMonocyteNatural killer T cellNeoplasmNeutrophilNonhumanOrgan transplantationPneumoniaPriority journalRegulatory T lymphocyteReviewSignal transductionT lymphocyteTissue injuryTissue reactionAdaptive immunityAnimalHumanImmunologyInnate immunityAdaptive ImmunityAnimalsHumansImmunity, InnatePurinesSignal TransductionReview10.1038/nri.2016.4