Table 1.

Influence of IFN-γ-signal deficiency on control of Plasmodium parasites in mice.

Plasmodium strain	Host mouse genotype (mAb administration)	Mouse background	Features of host mice after the Plasmodium infection	Reference
P. yoelii 17XNL	IFN-γ KO	B6/129	Delayed elimination of parasites and had higher parasitemia	van der Heyde et al. (37)
P. chabaudi adami 556KA	IFN-γ KO	B6/129	Delayed elimination of parasites and had higher parasitemia	van der Heyde et al. (37)
P. chabaudi chabaudi AS	IFN-γR KO IFN-γ KO	B6/129 B6	Higher parasitemia during second peak. 77% of the infected mice died Male mice developed higher parasitemia. Female mice delayed elimination of parasites and had higher parasitemia. 100% Male and 40% female mice died	Favre et al. (36), Su and Stevenson (39)
P. berghei XAT	WT (anti-IFN-γ mAb) IFN-γ KO	CBA B6	Could not eliminate parasites and died	Waki et al. (33), Yoneto et al. (35)
P. berghei NK65	WT (anti-IFN-γ mAb) WT (anti-IFN-γ mAb)	CBA B6	P. berghei NK65 is a high virulent strain and induces liver injury in CBA and B6 mice. The mAb-treated mice prolonged survival	Waki et al. (33), Yoshimoto et al. (34)
P. berghei ANKA	IFN-γR KO IFN-γ KO IFN-γR KO	CBAB6B6/129	P. berghei ANKA is a high virulent strain and induces neurological symptoms in 129 and B6 mice. The KO mice prolonged survival and did not developed neurological symptoms	Amani et al. (38), Villegas-Mendez et al. (61), Rudin et al. (94)

IFN, interferon; IFN-γR, IFNγ receptor; mAb, monoclonal antibody.