The myeloid type I interferon response to myocardial infarction begins in bone marrow and is regulated by Nrf2-activated macrophages
David Calcagno, Richard P Ng, Avinash Toomu, Claire Zhang, Kenneth Huang, Aaron D. Aguirre, Ralph Weissleder, Lori B. Daniels, Zhenxing Fu, Kevin R. King
Abstract
steady-state cardiac macrophages. Our results show that IFN signaling begins in the bone marrow, implicate multiple transcriptional regulators (Tet2, Irf3, and Nrf2) in governing ISG expression, and provide a clinical biomarker (ISG score) for studying IFN signaling in patients.
Topics & Concepts
IRF3Innate immune systemBone marrowMyeloidBiologyInterferonImmunologyProgenitor cellInflammationMonocyteCell biologyImmune systemTranscriptomeCancer researchStem cellGene expressionGeneBiochemistryNeutrophil, Myeloperoxidase and Oxidative MechanismsAtherosclerosis and Cardiovascular DiseasesCardiac Fibrosis and Remodeling