ing both IFNγ and perforin (IFNγ−/−Prf1−/−) still develop a severe MAS-like disease that requires the IL-33–ST2 axis and is downstream mediated by GM-CSF-producing CD8+ T cells. The inflammatory burden in infected IFNγ−/−Prf1−/− mice is even higher than in Prf1−/− mice, being characterised by a 10–15 times increase in neutrophils and stronger upregulation of IL-1β and IL-6.32 The same interplay bet