Transfer of adult IL-12^+/+ but not IL-12^−/− DCs into newborn mice down-regulates IL-13Rα1 expression, inhibits apoptosis, and restores secondary Th1 IFN-γ responses. Newborn (1-d-old) BALB/c mice were given 3 × 10⁴ neonatal DO11.10 T cells without (Nil) or with 2 × 10⁵ splenic DCs from adult wild-type (IL-12^+/+ DCs) or IL-12–deficient (IL-12^−/− DCs) BALB/c mice (reference 20) and were injected 1 d later with 100 μg Ig-OVA. After 7 wk, the mice were challenged with 125 μg OVA peptide in CFA, and 10 d later, the splenic cells (10⁶ cells/well) were stimulated with 10 μM OVA peptide for 24 h. (A–C) Apoptosis of KJ1-26⁺/IFN-γ⁺ Th1 cells was evaluated by staining with Annexin V, as described in Fig. 3. (D) Groups of mice were killed 2 wk after T cell/DC transfer and exposure to Ig-OVA, and primary Th1 cells were isolated using IFN-γ secretion kit, as described in Materials and methods. RNA was then extracted and IL-13Rα1 expression was determined by spot blot, as in Fig. 2. Because IL-13Rα1 mRNA parallels with protein expression (see Figs. 2, 3, and 4), all follow-up experiments will use mRNA analysis on separated Th1 cells. (E) IFN-γ production was measured using ELISPOT assay. Each bar represents the mean ± SD of duplicate spots.