Fig. 7

JAK1 inhibition prevents excessive IL-2 signaling and Th2 cell polarization in the absence of IL-6 signaling. A–I WT and Il6^-/- mice were transferred with OTII.4get cells, i.n. treated with HDM or HDM^LPS + OVA, orally treated with 20 mg/kg/day JAK1 inhibitor upadacitinib or vehicle at the indicated time points and analyzed on Day 3 (A–E) and Day 5 (F–I). Frequencies and numbers of total (C, H), CD25⁺ (B, D), pSTAT5⁺ (B, E), and IL-4-GFP⁺ (G, I) OTII cells in the mLN. (J–L) WT:Lck^cre-Il6r^fl/fl chimeras were i.n. sensitized with HDM or HDM^LPS, orally treated with upadacitinib or vehicle, and i.n. challenged with HDM (J). Frequencies of IL-13⁺ cells in the WT and Lck^cre-Il6r^fl/fl CD44^hiCD4⁺ T-cell compartments in the lungs (K, L). Data are representative of two independent experiments (mean±S.D., n = 5, one-way ANOVA)