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(Circulation Research. 2001;89:850.)
© 2001 American Heart Association, Inc.

Editorials

Nuclear Factor-B Decoy

Infiltrating the Heart of the Matter in Inflammatory Heart Disease

Peter P. Liu, Jenny Le, Min Nian

From the Heart & Stroke/Richard Lewar Centre of Excellence, University of Toronto; and Division of Cardiology, Toronto General Hospital, University Health Network, Toronto, Canada.

Correspondence to Dr Peter Liu, Heart & Stroke/RL Centre of Excellence, EN12-324, Toronto General Hospital, 200 Elizabeth St, Toronto, Ontario, M5G 2C4, Canada. E-mail peter.liu@utoronto.ca

See related article, pages 899–906

Key Words: myocarditis • inflammation • nuclear factor-B • transcription factor • molecular decoy

Inflammation is part of the host response repertoire in defense against injury. Inflammatory processes play an important role in all the common cardiovascular diseases such as atherosclerosis, myocardial infarction, and heart failure. However, when the inflammatory process becomes uncontrolled, it can become part of the disease. This situation is best exemplified by inflammatory heart diseases such as viral or autoimmune myocarditis, where the immune system can be triggered by either external antigens such as a virus, or internal antigens such as myosin. The activated immune cells then undergo exuberant signal amplification, leading to clonal expansion of T lymphocytes and elaboration of cytokines, resulting in cell and matrix disruption and the phenotype of dilated cardiomyopathy. ^1,2

Giant cell myocarditis is an example of disproportionate immune response, including coalescence of macrophages into giant cells mixed with lymphocytes, with associated high mortality and no specific treatment. To understand the pathogenesis of giant cell myocarditis, an experimental model of autoimmune myocarditis (EAM) induced by myosin antigen mixed with adjuvant in the murine model has been previously developed. ^3,4 The myosin molecule contains a very specific epitope of approximately 8 amino acids in size that can also be mimicked by infectious agents, which is capable of triggering immune cell activation in an MHC-restricted context, leading to T cell–mediated destruction of the myocardium (Figure 1). This has been definitively demonstrated by humanized murine models in which the mouse MHC system has been substituted with the human homologues, and the disease can be perfectly reproduced with immunogens . . . [Full Text of this Article]

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