Myocardial inflammation is tightly regulated by mechanisms including strong central and peripheral T cell tolerance and anti-inflammatory feedback involving cytokines such as interferon-gamma.
Because of the anatomy, function, and nonregenerative nature of the myocardium, inflammation in this tissue is not well tolerated. Nevertheless, various diseases of the heart are characterized by inflammatory responses involving the effector mechanisms of innate and adaptive (lymphocyte-dependent) immunity. The innate immune response to ischemia-reperfusion injury is, by far, the most common cause of myocardial inflammation. Innate responses may have beneficial influences that preserve myocardial function in the short term but may be maladaptive in chronic states. Adaptive responses in the myocardium occur with infection or loss of tolerance, and lead to myocarditis. Given the narrow margin for benefit of cardiac inflammation, special regulatory mechanisms likely raise the threshold, compared to other tissues, for the induction and persistence of adaptive immune responses. These mechanisms include strong central and peripheral T cell tolerance to heart antigens and induction of anti-inflammatory feedback mechanisms involving cytokines such as interferon-gamma.
Taqueti et al. (Wed,) conducted a review in Myocardial inflammation. Myocardial inflammation is tightly regulated by mechanisms including strong central and peripheral T cell tolerance and anti-inflammatory feedback involving cytokines such as interferon-gamma.
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