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Here, using mouse models of experimental autoimmune myocarditis (EAM) we investigated the role of heart non-specific CD4<jats:sup>+<\/jats:sup>T cells in the progression of the disease. Heart non-specific CD4<jats:sup>+<\/jats:sup>T cells were obtained from DO11.10 mice expressing transgenic T cell receptor recognizing chicken ovalbumin. We found that heart infiltrating CD4<jats:sup>+<\/jats:sup>T cells expressed exclusively effector (<jats:italic>T<\/jats:italic><jats:sub>eff<\/jats:sub>) phenotype in the EAM model and in hearts of patients with lymphocytic myocarditis. Adoptive transfer experiments showed that while heart-specific<jats:italic>T<\/jats:italic><jats:sub>eff<\/jats:sub>infiltrated the heart shortly after injection, heart non-specific<jats:italic>T<\/jats:italic><jats:sub>eff<\/jats:sub>effectively accumulated during myocarditis and became the major heart-infiltrating CD4<jats:sup>+<\/jats:sup>T cell subset at later stage. Restimulation of co-cultured heart-specific and heart non-specific CD4<jats:sup>+<\/jats:sup>T cells with\u00a0alpha-myosin heavy chain antigen showed mainly Th1\/Th17 response for heart-specific<jats:italic>T<\/jats:italic><jats:sub>eff<\/jats:sub>and up-regulation of a distinct set of extracellular signalling molecules in heart non-specific<jats:italic>T<\/jats:italic><jats:sub>eff<\/jats:sub>. Adoptive transfer of heart non-specific<jats:italic>T<\/jats:italic><jats:sub>eff<\/jats:sub>in mice with myocarditis did not affect inflammation severity at the peak of disease, but protected the heart from adverse post-inflammatory fibrotic remodelling and cardiac dysfunction at later stages of disease. Furthermore, mouse and human<jats:italic>T<\/jats:italic><jats:sub>eff<\/jats:sub>stimulated in vitro with common gamma cytokines suppressed expression of profibrotic genes, reduced amount of \u03b1-smooth muscle actin filaments and decreased contraction of cardiac fibroblasts. In this study, we provided a proof-of-concept that heart non-specific<jats:italic>T<\/jats:italic><jats:sub>eff<\/jats:sub>cells could effectively contribute to myocarditis and protect the heart from the dilated cardiomyopathy outcome.<\/jats:p>","DOI":"10.1007\/s00395-019-0766-6","type":"journal-article","created":{"date-parts":[[2019,12,20]],"date-time":"2019-12-20T13:02:53Z","timestamp":1576846973000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Heart non-specific effector CD4+ T cells protect from postinflammatory fibrosis and cardiac dysfunction in experimental autoimmune myocarditis"],"prefix":"10.1007","volume":"115","author":[{"given":"Martina","family":"Zarak-Crnkovic","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabriela","family":"Kania","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Agnieszka","family":"Ja\u017awa-Kusior","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcin","family":"Czepiel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Winandus J.","family":"Wijnen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jaros\u0142aw","family":"Czy\u017c","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bj\u00f6rn","family":"M\u00fcller-Edenborn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daria","family":"Vdovenko","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diana","family":"Lindner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cristina","family":"Gil-Cruz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marta","family":"Bachmann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dirk","family":"Westermann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Burkhard","family":"Ludewig","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oliver","family":"Distler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas F.","family":"L\u00fcscher","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karin","family":"Klingel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Urs","family":"Eriksson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2521-3232","authenticated-orcid":false,"given":"Przemys\u0142aw","family":"B\u0142yszczuk","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2019,12,20]]},"reference":[{"issue":"3","key":"766_CR1","doi-asserted-by":"publisher","first-page":"19","DOI":"10.1007\/s00395-019-0722-5","volume":"114","author":"L Bacmeister","year":"2019","unstructured":"Bacmeister L, Schwarzl M, Warnke S, Stoffers B, Blankenberg S, Westermann D, Lindner D (2019) Inflammation and fibrosis in murine models of heart failure. 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