IL33 and myocarditis: This scenario, losing regulatory populations while gainingand activating pathogenic ones, differs from other models of infectiousmyocarditis, where an increase in almost all macrophage subsets canbe observed. Neutrophils, although notincreased in number, acquired a hyperactivated phenotype with elevatedIL-17, IFN-γ, and MHC-II expression, paralleling reports thatactivated neutrophils exacerbate myocarditis in infectious and immunecontexts. Together, these alterationssuggest that IL-33/ST2 signaling normally restrains pro-inflammatoryactivation across multiple myeloid compartments.