Activated regulatory T-cells attenuate myocardial ischaemia/reperfusion injury through a CD39-dependent mechanism

Regulatory T lymphocytes (Tregs) are regarded as key immunomodulators in immune-mediated disorders. Our data validated a protective role of Tregs in myocardial ischemia reperfusion injury (MIRI). Moreover, activated Tregs ameliorated MIRI via a CD39-dependent mechanism, representing a putative therapeutic strategy. Abbreviations: AAR, area at risk; Ab, antibody; AMI, acute myocardial infarction; BAC, bacterial artificial Chromsomes; CCR5, C-C chemokine receptor type 5; CD, cluster of differentiation; cTnT, cardiac troponin T; CXC, cysteine-X-cysteine; DEREG, depletion of regulatory T-cell; DT, diphtheria toxin; EF, ejection fraction; ELR, glutamic acid–leucine-arginine; ERK, extracellular-signal-regulated kinase; Foxp3, Forkhead box P3; FS, fractional shortening; GVHD, graft-versus-host disease; I/R, ischaemia/reperfusion; IL, interleukin; IRI, ischaemia/reperfusion injury; KC, cytokine-induced neutrophil chemoattractant; LAD, left anterior descending; LIX, lipopolysaccharide-induced CXC chemokine; LPS, lipopolysaccharide; LV, left ventricle/ventricular; mAb, monoclonal antibody; MIP, macrophage inflammatory protein; MIRI, myocardial ischaemia/reperfusion injury; MPO, myeloperoxidase; PCI, percutaneous coronary intervention; RISK, reperfusion injury salvage kinase; STEMI, ST-elevation myocardial infarction; TGF, transforming growth factor; Tregs, regulatory T-cells; TUNEL, terminal deoxynucleotidyltransferase mediated dUTP nick-end labeling; Th, T-helper; Treg, regulatory T-cell; WT, wild-type