IFNγ protected against the development of severe chronic myocarditis, pericarditis, and dilated cardiomyopathy after infection with Coxsackievirus B3, reducing mast cell degranulation, volume of fibrous myocardial tissue and production of profibrotic cytokines such as TGFb, IL-1b and IL-4 [81]. Here, IL1B is linked to infection.