Document Type

Article

Publication Date

2-23-2021

Keywords

JMG

JAX Source

Circulation 2021 Feb 23; 143(8):821-836

Volume

143

Issue

8

First Page

821

Last Page

836

ISSN

1524-4539

PMID

33297741

DOI

https://doi.org/10.1161/circulationaha.120.044581

Abstract

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

Comments

We gratefully acknowledge the contribution of Stephen Rothery and the Facility for Imaging and Light Microscopy (FILM) at Imperial College London, Elaine Bechtel and the Histology and Light Microscopy Scientific Services, and William Schott at the Flow Cytometry Service at The Jackson Laboratory for expert assistance with the work described in this publication. We are grateful for technical advice and support from Michael M. Mclellan (The Jackson Laboratory).

This is an open access article under the terms of the Creative Commons Attribution License.

Download

Share

COinS