Circulation 2021 Feb 23; 143(8):821-836
BACKGROUND: Ischemic heart disease is a leading cause of heart failure and despite advanced therapeutic options, morbidity and mortality rates remain high. Although acute inflammation in response to myocardial cell death has been extensively studied, subsequent adaptive immune activity and anti-heart autoimmunity may also contribute to the development of heart failure. After ischemic injury to the myocardium, dendritic cells (DC) respond to cardiomyocyte necrosis, present cardiac antigen to T cells, and potentially initiate a persistent autoimmune response against the heart. Cross-priming DC have the ability to activate both CD4
METHODS: We induced type 2 myocardial infarction-like ischemic injury in the heart by treatment with a single high dose of the β-adrenergic agonist isoproterenol. We characterized the DC population in the heart and mediastinal lymph nodes and analyzed long-term cardiac immunopathology and functional decline in wild type and
RESULTS: A diverse DC population, including cross-priming DC, is present in the heart and activated after ischemic injury.
CONCLUSION: Activation of cytotoxic CD8
Forte, Elvira; Perkins, Bryant; Sintou, Amalia; Kalkat, Harkaran S; Papanikolaou, Angelos; Jenkins, Catherine; Alsubaie, Mashael; Chowdhury, Rasheda A; Duffy, Theodore M; Skelly, Daniel A; Branca, Jane; Bellahcene, Mohamed; Schneider, Michael D; Harding, Sian E; Furtado, Milena B; Ng, Fu Siong; Hasham, Muneer G.; Rosenthal, Nadia; and Sattler, Susanne, "Cross-Priming Dendritic Cells Exacerbate Immunopathology After Ischemic Tissue Damage in the Heart." (2021). Faculty Research 2021. 45.