Figure 4
Figure 4. Disruption of anti-FrCasE immune response in infected/667-treated mice on transfer of Tregs from infected/nontreated mice. (A) Experimental design. Mice were infected neonatally and immunotherapy treated with 667. They were virally challenged at 8 weeks of age and subjected to adoptive transfer with purified Tregs (3 × 105 cells) from various origins before analysis of humoral and CTL immune responses, conducted as in Figure 3. Tregs were purified from 8-week-old noninfected/nontreated, infected/nontreated, infected/667-treated, infected/667-F(ab′)2–treated, or infected/672-treated mice. (B) Assay of GagL-specific CD8+ T cells. (C) In vivo assay of anti-FrCasE–infected cell CTL responses. (D) Assay of anti-FrCasE IgGs. For panels B, C and D, 3 independent experiments with 3 mice per group were conducted. Data are presented as means ± SEM. The statistical significance between groups was established using the Student t test. *P < .05.

Disruption of anti-FrCasE immune response in infected/667-treated mice on transfer of Tregs from infected/nontreated mice. (A) Experimental design. Mice were infected neonatally and immunotherapy treated with 667. They were virally challenged at 8 weeks of age and subjected to adoptive transfer with purified Tregs (3 × 105 cells) from various origins before analysis of humoral and CTL immune responses, conducted as in Figure 3. Tregs were purified from 8-week-old noninfected/nontreated, infected/nontreated, infected/667-treated, infected/667-F(ab′)2–treated, or infected/672-treated mice. (B) Assay of GagL-specific CD8+ T cells. (C) In vivo assay of anti-FrCasE–infected cell CTL responses. (D) Assay of anti-FrCasE IgGs. For panels B, C and D, 3 independent experiments with 3 mice per group were conducted. Data are presented as means ± SEM. The statistical significance between groups was established using the Student t test. *P < .05.

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