IL-33, an alarmin cytokine released upon tissue damage, signalsthrough its receptor ST2 to exert pleiotropic effects that can beeither protective or pathological. Inthe heart, IL-33 has been shown to limit myocarditis by dampeningTh1 responses and promoting IL-4 production by macrophages, and Tcells. In helminth infections, dysregulationof this axis has been associated with uncontrolled Th1/Th17 activityand impaired regulatory T cell responses., Yet, its role in shaping the cardiac immunopathology of T. cruzi infection has remained unresolved. Here, IL33 is linked to myocarditis.