Abstract
Experimental autoimmune myocarditis (EAM) represents a CD4+ T cell-mediated mouse model of inflammatory heart diseases. Genetically susceptible mice injected with cardiac self-antigen-loaded dendritic cells or immunized with cardiac self-antigen together with strong adjuvants develop overt cardiac inflammation. Later on, affected mice develop heart failure and a cardiac phenotype, which closely resembles the morphological picture of dilated cardiomyopathy in humans. IL-17-producing T cells contribute to EAM development, but the absence of IL-17A signaling on CD4+ T cells can be compensated by other heart-reactive T helper cell subsets. IL-17A, however, has proven to be critical for progression of acute myocarditis to an end-stage heart failure phenotype. Accordingly, cytokines promoting Th17 CD4+ expansion and/or IL-17 release, such as IL-23, IL-6, TGF-β, and IL-1, are key players in EAM and most likely in inflammatory dilated cardiomyopathy. Understanding the specific role of distinct cytokines during induction and progression of EAM will expand our knowledge on the pathogenesis of dilated cardiomyopathy and will help us to develop novel treatment strategies in the future.
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Acknowledgment
Urs Eriksson acknowledges support from Medtronik, Boston Scientific, Novartis, the Swiss Heart Foundation, and from the Swiss National Foundation.
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Eriksson, U. (2013). The Role of IL-17 in Experimental Autoimmune Myocarditis. In: Quesniaux, V., Ryffel, B., Padova, F. (eds) IL-17, IL-22 and Their Producing Cells: Role in Inflammation and Autoimmunity. Progress in Inflammation Research. Springer, Basel. https://doi.org/10.1007/978-3-0348-0522-3_12
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