Figure 3

Tyk-2^(−/−) mice showed a defective Th17 cytokine production in vivo.

(a). and (b). Mice were treated with OVA as described in the methods section. After 21 days the mice were sacrificed and total cells were isolated from the lung. After 24 h incubation with antibodies against CD3 and CD28 supernatants were analyzed by ELISA for IL-17A ((a): n = 2–4, p = 0,041; p = 0,007) and IL-17F ((b): n = 2–4, p = 0,046, p = 0,046). (c). Total lung cells from untreated mice were isolated and incubated with antibodies against CD4 and IL-17A and analyzed by flow cytometry. Data show on the one hand, lung IL-17A⁺CD4⁺ T cells (left panel n = 3–4, p = 0,0003) and on the other hand lung IL-17A⁺CD4⁻ cells (right panel n = 3–4, p = 0,003). (d). Total lung cells from naïve and allergen-treated mice were incubated with α-CD3 and α-CD28 antibodies for 24 h and analyzed by ELISA for IL-1β production (n = 2–4, p = 0,009). (e). and (f). IL-21(n = 4–5, p = 0,025; p = 0,0019; p = 0,041; p = 0,002) and IL-23 (n = 3–5, p = 0,045; p = 0,038; p = 0,043; p = 0,012) levels were measured in the BALF of naïve and asthmatic mice.