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Here, we show that following acute myocardial infarction in mice, CD8\n                    <jats:sup>+<\/jats:sup>\n                    T lymphocytes are recruited and activated in the ischemic heart tissue and release Granzyme B, leading to cardiomyocyte apoptosis, adverse ventricular remodeling and deterioration of myocardial function. Depletion of CD8\n                    <jats:sup>+<\/jats:sup>\n                    T lymphocytes decreases apoptosis within the ischemic myocardium, hampers inflammatory response, limits myocardial injury and improves heart function. These effects are recapitulated in mice with\n                    <jats:italic>Granzyme B<\/jats:italic>\n                    -deficient CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells. The protective effect of CD8 depletion on heart function is confirmed by using a model of ischemia\/reperfusion in pigs. Finally, we reveal that elevated circulating levels of GRANZYME B in patients with acute myocardial infarction predict increased risk of death at 1-year follow-up. Our work unravels a deleterious role of CD8\n                    <jats:sup>+<\/jats:sup>\n                    T lymphocytes following acute ischemia, and suggests potential therapeutic strategies targeting pathogenic CD8\n                    <jats:sup>+<\/jats:sup>\n                    T lymphocytes in the setting of acute myocardial infarction.\n                  <\/jats:p>","DOI":"10.1038\/s41467-021-21737-9","type":"journal-article","created":{"date-parts":[[2021,3,5]],"date-time":"2021-03-05T06:03:22Z","timestamp":1614924202000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":211,"title":["Cytotoxic CD8+ T cells promote granzyme B-dependent adverse post-ischemic cardiac 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