IFNG and Atherosclerotic lesion: Although ATP6V0d2 does not participate in parasite resistance to the classical in vitro IFN-γ/LPS model of inflammatory macrophages, this V-ATPase subunit isoform was required for parasite survival in macrophages stimulated with ox-LDL, a potent inflammatory stimulus mainly studied in the context of atherosclerotic lesions but that has also been implicated in chronic psoriatic skin inflammation [71, 72].