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. Author manuscript; available in PMC: 2016 Jul 15.
Published in final edited form as: J Immunol. 2015 Jun 1;195(2):507–518. doi: 10.4049/jimmunol.1500027

Figure 8.

Figure 8

IL-4 from basophils modulates IL-12 production by DCs to sustain control of primary Th1 immunity in the newborn. (A) Neonatal MHC-II−/− IL-13Rα1+/+ mice (3 per group) recipient of basophils and DCs from 1-day-old IL-13Rα1+/+ (HR+BA: HR+DC) or IL-13Rα1−/− (HR−BA:HR−DC) mice were given neonatal DO11.10 CD4+ T cells and injected with Ig-OVA. On day 14, the SP cells were harvested and incubated with OVAp-loaded MHC-II+/+ DCs (to serve as APCs). IFNγ and IL-4 production by KJ1-26+CD4+ DO11.10 T cells were measured by ELISPOT. The bars represent the mean ± SD spot forming units (SFU) of triplicate wells. The results are representative of 3 independent experiments. (B) shows IL-12 production by IL-13Rα1−/− and IL-13Rα1+/+ DCs upon stimulation with control media (NIL), LPS alone, or in combination with rIL-4 cytokine (left panel). Each bar represents the mean ± SD of triplicate wells. The right panel shows the fold change in IL-12 production by IL-13Rα1+/+ and IL-13Rα1−/− DCs induced by exogenous IL-4. Each bar represents the mean ± SE of cytokine production ratio obtained upon stimulation in the presence versus absence of IL-4. The data is derived from 3 experiments.