CD69 Limits the Severity of Cardiomyopathy After Autoimmune Myocarditis

Circulation, 09/21/2010

The findings indicate that CD69 negatively regulates heart–specific Th17 responses, cardiac inflammation, and heart failure progression in experimental autoimmune myocarditis.

Author Commentary

The mechanisms involved in the immune activation observed during the progression of human chronic heart failure and dilated cardiomyopathy have not been fully elucidated . However, a number of recent studies suggest that, besides genetic susceptibility and infections, chronic immune-mediated inflammation after acute myocarditis may lead to dilated cardiomyopathy. This report investigates the role of the leukocyte activation antigen CD69 in the modulation of the inflammatory response in a mouse model of autoimmune myocarditis. Our data demonstrate that CD69, through the regulation of Th17 effector responses, limits myocardial inflammation and subsequent heart failure. It is very feasible that a similar phenomenon occurs in humans with myocarditis and subsequent dilated cardiomyopathy . These findings reveal the involvement of a novel molecular actor in the immunopathogenesis of myocarditis, which could be a potential therapeutic target.

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