Key result
In a murine model of myocarditis, disease progression is promoted by complement, TNF-alpha, IL-4, and IL-12, and suppressed by IFN-gamma, IL-10, and CTLA-4.
Does not support clinical immunomodulation in myocarditis; leaves open human validation of these murine immune pathways.
Cardiac myosin-induced murine myocarditis provides a useful model for assessing the role of immune mediators in the development of inflammatory heart disease. Myocarditis is characterized by leucocyte infiltration, fibrosis, and cardiomyocyte death, which collectively lead to deterioration of both systolic and diastolic function as assessed by pressure-volume relations. In severe cases, disease progresses to dilated cardiomyopathy and heart failure. Key factors that promote disease include complement, tumour necrosis factor-alpha, interleukin-4, and interleukin-12. Factors found to supress myocarditis include interferon-gamma, interleukin-10, and cyotoxic T lymphocyte antigen-4. Final disease outcome is determined by the interplay of these immune mediators.
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Marina Afanasyeva (2002) conducted a review in Inflammatory heart disease (Myocarditis). Immune mediators was evaluated. In a murine model of myocarditis, disease progression is promoted by complement, TNF-alpha, IL-4, and IL-12, and suppressed by IFN-gamma, IL-10, and CTLA-4.
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