volume 191, issue 8, P4038-4047 2013
DOI: 10.4049/jimmunol.1301282
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Jobert G. Barin, G. Christian Baldeviano, Monica V. Talor, Lei Wu, SuFey Ong, DeLisa Fairweather, Djahida Bedja, Natalie R. Stickel, Jillian A. Fontes, Ashley B. Cardamone, Dongfeng Zheng, Kathleen L. Gabrielson, Noel R. Rose, Daniela Čiháková et al.

Abstract: CD4+ T cells play a central role in inflammatory heart disease, implicating a cytokine product associated with helper T cell effector function as a necessary mediator of this pathophysiology. IFNγ-deficient mice developed severe autoimmune myocarditis (EAM), in which mice are immunized with cardiac myosin peptide, while IL17A-deficient mice were protected from progression to dilated cardiomyopathy. We generated IFNγ−/−IL17A−/− mice to assess whether IL17 signaling was responsible for the severe EAM of IFNγ−/−…

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