Hypoxia/Reoxygenation Inhibits P2Y11 Receptor Expression and Its Immunosuppressive Activity in Human Dendritic Cells

摘要: High concentrations of extracellular ATP (eATP) resulting from cell damage may be found during an ischemia/reperfusion (I/R) episode at the site injury. eATP activates purinergic receptors in dendritic cells (DCs) and inhibit inflammation. This immunosuppressive activity could interest field I/R, which is inflammatory condition involved myocardial infarction, stroke, solid organ transplantation. However, specific receptor responsible for this effect remains to identified. In study, we report that induced maturation human monocyte-derived DCs. Additionally, inhibited IL-12 production whereas IL-10 levels remained unchanged activated These effects were prevented by P2Y11R antagonist NF340. Interestingly, a 5-h hypoxia on cytokine 1-h did not affect eATP-mediated decrease IL-6. We showed time-dependent downregulation both mRNA protein was knocking down hypoxia-inducible factor-1α. role demonstrated orientates DCs toward proinflammatory phenotype post-I/R injuries as observed after