Mast cells, but not FcRγ-dependent signaling, promote Th17-mediated neutrophilic airway inflammation. Mice were treated with 50 μg of OVA or PBS intranasally for 3 days (once per day). Cells in BALF were quantified 24 hours after the last OVA or PBS inhalation. (A) FcRγ^+/+ OTII mice (PBS, n = 8; OVA, n = 14), and FcRγ^−/− OTII mice (PBS, n = 7; OVA, n = 14). (B) Kit^+/+ OTII mice (PBS, n = 18; OVA, n = 24), Kit^W/W-v OTII mice (PBS, n = 7; OVA, n = 14) and Kit^W/W-v OTII mice which were systemically engrafted with Kit^+/+ BMCMCs (Kit^W/W-v OTII + WT BMCMCs) (PBS, n = 7; OVA, n = 14). *P < .01 versus corresponding values for PBS-treated mice; †P < .01 versus corresponding values for OVA-treated Kit^+/+ OTII mice or OVA-treated Kit^W/W-v OTII mice plus WT BMCMCs (B). Data are the average + SD of results pooled from 3 independent experiments, all of which gave similar results.