This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Cunningham, M. W. Search for Related Content PubMed PubMed Citation Articles by Cunningham, M. W. Related Collections Related Article

(Circulation Research. 2006;99:1024.)
© 2006 American Heart Association, Inc.

Editorials

T Regulatory Cells

Sentinels Against Autoimmune Heart Disease

Madeleine W. Cunningham

From the University of Oklahoma Health Sciences Center, Biomedical Research Center, Oklahoma City.

Correspondence to Madeleine W. Cunningham, PhD, George Lynn Cross Research Professor, Microbiology and Immunology, University of Oklahoma Health Sciences Center, Biomedical Research Center, 975 NE 10^th Street, Oklahoma City, OK 73104. Email madeleine-cunningham@ouhsc.edu

See related article, pages 1109–1116

Key Words: autoimmunity • myocarditis • coxsackievirus • T lymphocytes • cardiomyopathy

An extract of the first 250 words of the full text is provided, because this article has no abstract.

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 ß-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 factor (TNF) transgenic mouse model of myocarditis as discussed below.¹⁹ Viral infection has long been associated with the development of myocarditis, of which the coxsackieviruses are reported frequently to be the infectious agent leading to acute myocarditis. It is striking that the new data . . . [Full Text of this Article]

Related Article:

Coxsackievirus B3 Induces T Regulatory Cells, Which Inhibit Cardiomyopathy in Tumor Necrosis Factor- Transgenic Mice

Sally A. Huber, Arthur M. Feldman, and Danielle Sartini
Circ. Res. 2006 99: 1109-1116. [Abstract] [Full Text] [PDF]