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DCMi develops in up to 30% of myocarditis patients, but the mechanisms involved in disease progression are poorly understood. Patients with eosinophilia frequently develop cardiomyopathies. In this study, we used the experimental autoimmune myocarditis (EAM) model to determine the role of eosinophils in myocarditis and DCMi. Eosinophils were dispensable for myocarditis induction but were required for progression to DCMi. Eosinophil-deficient \u0394dblGATA1 mice, in contrast to WT mice, showed no signs of heart failure by echocardiography. Induction of EAM in hypereosinophilic IL-5Tg mice resulted in eosinophilic myocarditis with severe ventricular and atrial inflammation, which progressed to severe DCMi. This was not a direct effect of IL-5, as IL-5Tg\u0394dblGATA1 mice were protected from DCMi, whereas IL-5\u2212\/\u2212 mice exhibited DCMi comparable with WT mice. Eosinophils drove progression to DCMi through their production of IL-4. Our experiments showed eosinophils were the major IL-4\u2013expressing cell type in the heart during EAM, IL-4\u2212\/\u2212 mice were protected from DCMi like \u0394dblGATA1 mice, and eosinophil-specific IL-4 deletion resulted in improved heart function. In conclusion, eosinophils drive progression of myocarditis to DCMi, cause severe DCMi when present in large numbers, and mediate this process through IL-4.<\/jats:p>","DOI":"10.1084\/jem.20161702","type":"journal-article","created":{"date-parts":[[2017,3,16]],"date-time":"2017-03-16T14:10:25Z","timestamp":1489673425000},"page":"943-957","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":105,"title":["Eosinophil-derived IL-4 drives progression of myocarditis to inflammatory dilated cardiomyopathy"],"prefix":"10.1084","volume":"214","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9145-5216","authenticated-orcid":true,"given":"Nicola L.","family":"Diny","sequence":"first","affiliation":[{"name":"W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G. 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