IFNG and parasitic infectious disease: Despite IL-12 administration rescuing TMCs, accelerating NK-derived IFN-γ kinetics, restoring cDC1s, and reducing parasite burden in infected Tbx21−/− mice (Fig. 2E, 2F, Supplemental Fig. 2C–F), it was insufficient to prevent their rapid mortality during T. gondii infection (Fig. 2G), suggesting that intrinsic T-bet expression by TMCs plays a role in host survival during parasite infection.