Open AccessCD73 on T Cells Orchestrates Cardiac Wound Healing After Myocardial Infarction by Purinergic Metabolic Reprogramming
Author(s) -
Nadine Borg,
Christina Alter,
Nicole Görldt,
Christoph Jacoby,
Zhaoping Ding,
Bodo Steckel,
Christine Quast,
Florian Bönner,
Daniela Friebe,
Sebastian Temme,
Ulrich Flögel,
Jürgen Schrader
Publication year - 2017
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.116.023365
Subject(s) - medicine , purinergic receptor , myocardial infarction , reprogramming , wound healing , cardiology , surgery , cell , adenosine , biology , genetics
T cells are required for proper healing after myocardial infarction. The mechanism of their beneficial action, however, is unknown. The proinflammatory danger signal ATP, released from damaged cells, is degraded by the ectonucleotidases CD39 and CD73 to the anti-inflammatory mediator adenosine. Here, we investigate the contribution of CD73-derived adenosine produced by T cells to cardiac remodeling after ischemia/reperfusion and define its mechanism of action.
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