Figure 7
Figure 7. CpG-ODN protects H-ras– and N-ras–deficient mice from L major infection. (A) Course of L major infection in CpG-ODN–treated WT, H-ras–, and N-ras–deficient mice. Mean induration ± SD of 2-3 mice (4-6 ears) per group are shown. Dotted line represents the evolution of infection in untreated WT mice. (B) Parasite burden per ear in infected CpG-ODN–treated mice at weeks 3 and 8 after infection. Results represent mean ± SD for 2 mice per group. (C) IFN-γ and IL-4 production, as determined by ELISA, by draining LN cells isolated from untreated (−) or CpG-ODN–treated (+) L major–infected mice at week 3 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 of untreated mice (*P < .01 and **P < .001 vs untreated WT) or 2 mice in the CpG-ODN–treated groups. IL-4 was not detectable in CpG-ODN–treated mice regardless of their genotype.

CpG-ODN protects H-ras– and N-ras–deficient mice from L major infection. (A) Course of L major infection in CpG-ODN–treated WT, H-ras–, and N-ras–deficient mice. Mean induration ± SD of 2-3 mice (4-6 ears) per group are shown. Dotted line represents the evolution of infection in untreated WT mice. (B) Parasite burden per ear in infected CpG-ODN–treated mice at weeks 3 and 8 after infection. Results represent mean ± SD for 2 mice per group. (C) IFN-γ and IL-4 production, as determined by ELISA, by draining LN cells isolated from untreated (−) or CpG-ODN–treated (+) L major–infected mice at week 3 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 of untreated mice (*P < .01 and **P < .001 vs untreated WT) or 2 mice in the CpG-ODN–treated groups. IL-4 was not detectable in CpG-ODN–treated mice regardless of their genotype.

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