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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Clin Exp Allergy. 2016 Feb;46(2):317–328. doi: 10.1111/cea.12612

Figure 2. IL-17A induced GMCSF production by HBEC requires EGFR signaling, and protease/TACE activity, and p38 MAPK signaling.

Figure 2

HBEC were stimulated with (A) IL-13 (100 ng), IL-17A (100 ng), or a combination of both IL-13 and -17A; (B) increasing amounts of IL-17A (1-100 ng); (C) IL-17A (25 ng) with or with the EGFR inhibitor Erlotinib (0.1 μM [+] or 0.25 μM [++]); (D) IL-17A (25 ng) with or without the protease inhibitor GM6001 (20 μM) or the TACE inhibitor TAPI-1 (20 μM); (E) IL-17A (25 ng) with or without the p38 inhibitor SB202190 (2 μM [+] or 5 μM [++]); (F) IL-17A (25ng) with or without neutralizing antibodies to AREG (0.3 μg/mL [+] or 1 μg/mL [++]). GMCSF was measured in the media by ELISA 24 hours after stimulation (A-F), and statistical significance was determined by comparing samples to the medium only group (* p<0.05, ** p<0.01, *** p<0.001) or compared to the IL-17A stimulated group (^^^ p<0.001); n=2 (two independent experiments, each performed in triplicate) for each group in (A-F).