Figure 5
Figure 5. H-ras and N-ras deficiency enhance susceptibility to L major infection. (A) Course of L major infection in WT, H-ras–, and N-ras–deficient mice. Mean lesion size ± SD of 4-10 mice per group are shown (*P < .001 and **P < .0005 vs WT). (B) Ear lesions with focal necrosis in infected Ras-deficient but not WT mice at week 12 after infection. (C) Parasite burden in the ear and draining LN (DLN) from infected mice at weeks 3 and 12 after infection. Results represent mean ± SD for 4 mice per group (**P < .0005 vs WT). (D) IFN-γ and IL-4 production, as determined by ELISA, by draining LN cells isolated from L major–infected mice at week 12 after infection and stimulated with SLA (12 μg/mL) for 48 hours. Values represent the mean ± SD of duplicate cultures and 4 mice in each group (*P < .001 and **P < .0005 vs WT). The data shown are representative of 2 independent experiments.

H-ras and N-ras deficiency enhance susceptibility to L major infection. (A) Course of L major infection in WT, H-ras–, and N-ras–deficient mice. Mean lesion size ± SD of 4-10 mice per group are shown (*P < .001 and **P < .0005 vs WT). (B) Ear lesions with focal necrosis in infected Ras-deficient but not WT mice at week 12 after infection. (C) Parasite burden in the ear and draining LN (DLN) from infected mice at weeks 3 and 12 after infection. Results represent mean ± SD for 4 mice per group (**P < .0005 vs WT). (D) IFN-γ and IL-4 production, as determined by ELISA, by draining LN cells isolated from L major–infected mice at week 12 after infection and stimulated with SLA (12 μg/mL) for 48 hours. Values represent the mean ± SD of duplicate cultures and 4 mice in each group (*P < .001 and **P < .0005 vs WT). The data shown are representative of 2 independent experiments.

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