T regulatory cells: sentinels against autoimmune heart disease.

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See related article, pages 1109–1116 Myocarditis is an acute inflammatory disease of the heart and a precursor of dilated cardiomyopathy.1–8 Dilated cardiomyopathy is a more chronic disease which is characterized by ventricular hypertrophy and which may be a direct result of myocarditis and lead to heart failure.1–3,9 Myocarditis is often characterized by a cellular infiltrate, and if inflammation of the myocardium does not resolve during the acute stage, the heart may be compromised because of necrosis and direct loss of myocytes,10 scarring from granulomatous inflammation,11,12 or fibrosis because of proliferation of fibroblasts and collagen deposition.13,14 Although TH1 or TH2 cell mediated immunity is blamed for disease, myocarditis has been reported to develop independently of TH1 and TH2 mechanisms.15 In some cases of myocarditis, antibody deposition and antibody-mediated cell signaling of the β-adrenergic receptor or the calcium channel may affect cardiomyocyte function and lead to cardiomyopathy or apoptosis in the myocardium.16–18 Whichever type of disease occurs, the myocardium may deteriorate from relapsing and remitting disease and become enlarged and functionally weakened because of the immune attack on the heart. In this issue of Circulation Research , Huber and colleagues report that a coxsackievirus variant can affect the outcome of myocarditis by inducing regulatory T cells which abrogate disease in the tumor necrosis …