摘要：SummaryExtracellular ATP released to the ischemic brain parenchyma is quickly metabolized by ectonucleotidases. Among them, the ecto-5′-nucleotidase CD73 encoded byNt5egenerates immunosuppressive adenosine. Genetic deletion ofNt5eled to increased infarct size in the murine photothrombotic stroke model. We aimed at validating this result using the transient middle cerebral artery occlusion (tMCAO) stroke model that represents pathophysiological aspects of penumbra and reperfusion. Three days after tMACO, we did not detect a difference in stroke size between CD73-deficient (CD73−/−) and control mice. Consistent with this finding, CD73−/−and control mice showed comparable numbers and composition of brain-infiltrating leukocytes measured by flow cytometry. Using NanoString technology, we further demonstrated that CD73−/−and control mice do not differ regarding glia cell gene expression profiles. Our findings highlight the potential impact of stroke models on study outcome and the need for cross-validation of originally promising immunomodulatory candidates.Graphical abstractDisplay OmittedHighlights•Infarct volume on day 3 after tMCAO was comparable among CD73−/−and control mice•Brain leukocyte infiltration on day 3 after tMCAO was similar in CD73−/−and control mice•Glial RNA expression profile on day 3 after tMCAO was similar in CD73−/−and control miceBiological sciences; Molecular biology; Immunology
