Transgenic expression of Nogo-B in lung epithelium inhibits allergic Th2 inflammation. (A) CCSP-Nogo-DTG mice were put on doxycycline water (0.5 mg/ml) for different time points and the levels of Nogo-B HA–tagged transgene assessed. Endogenous mouse Nogo-B and hsp90 levels were used as loading controls. Each lane represents lung lysate from an individual mouse and was repeated one additional time. (B) Transgene expression in lung sections from CCSP-Ng-DTG mice. Bars, 100 µm. (C) CCSP-Ng-STG and DTG littermates were put on doxycycline water for 7 d before OVA sensitization/challenge. Lung sections from control and OVA-sensitized and challenged STG and DTG mice were stained for transgene expression (a and b, and c and d, respectively), Nogo-A/B (e and f), H&E (g and h), and PAS (I and j). Arrowheads highlight airway epithelium. Bar, 200 µm. (D and E) BAL cell counts (D) and levels of cytokines (E) were evaluated from BAL of OVA STG and DTG mice (*, P < 0.05). (F) WT OTII CD4⁺ Th2 cells were purified and adoptively transferred into STG and DTG mice, followed by OVA challenge and evaluation of total levels of inflammation in the BAL (*, P < 0.05). Data are expressed as the mean ± SEM. n = 5–8 mice for both groups representative of three individual experiments.