Research ArticleINFLAMMATION

The myeloid type I interferon response to myocardial infarction begins in bone marrow and is regulated by Nrf2-activated macrophages

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Science Immunology  25 Sep 2020:
Vol. 5, Issue 51, eaaz1974
DOI: 10.1126/sciimmunol.aaz1974

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Cardioprotective myeloid cells

Acute ischemic injury to the heart precipitates a strong inflammatory response including influx of myeloid cells expressing type I interferon–stimulated genes (ISGs). Calcagno et al. used single-cell RNA sequencing to probe the origin, evolution, and heterogeneity of this response in the first 4 days after myocardial infarction using human and mouse myeloid cells. Induction of ISG in myeloid cells was initially observed in bone marrow and blood. Post-infarct cardiac tissue in mice contained myeloid subsets with and without ISG expression and a steady-state macrophage population with Nrf2-dependent anti-inflammatory activity. On the basis of their findings, the authors developed an ISG score as a potential biomarker to assess how the vigor of type I interferon signaling influences clinical outcomes after a heart attack.

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