Consistent with the finding that resistance to infection could be restored in these mice by dampening inflammation through NLRP3/IL-1β blocking (de Luca et al, 2014; Iannitti et al, 2016), Tβ4 down-regulated NLRP3 expression in these mice (Fig 3E) and, accordingly, reduced IL-1β, along with TNF-α, IL-17A, and increased IFN-γ production, an effect negated upon siHif1α treatment (Fig 3F). Here, IFNG is linked to infection.