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. Author manuscript; available in PMC: 2012 Oct 1.
Published in final edited form as: Nat Med. 2012 Mar 4;18(4):547–554. doi: 10.1038/nm.2684

Figure 3. IL-17A-mediated enhanced ASM contraction is not due to contaminants or TNF-α release.

Figure 3

(a) Contractile force measurements from mouse tracheal rings treated for 12 hours with or without 100 ng ml−1 IL-17A in the presence of 1μM atropine and stimulated with methacholine MCh or KCl. (b) Contractile force measurements from tracheal rings stimulated with MCh or KCl after treatment for 12 hours with or without 100 ng ml−1 IL-17A in the presence of 40 μg ml−1 IL-17 neutralizing antibodies or isotype control antibodies. (c) Contractile force measurements from tracheal rings stimulated with MCh or KCl after treatment for 12 hours with or without 100 ng ml−1 IL-17A in the presence of 40 μg ml−1 TNF-α neutralizing antibodies or isotype control antibodies. (d) Contractile force measurements from tracheal rings stimulated with MCh or KCl after treatment for 12 hours with or without 100 ng ml−1 TNF-α in the presence of 40 μg ml−1 TNF-α neutralizing antibodies or isotype control antibodies. *P < 0.05, **P < 0.01 and ***P < 0.001 in IL-17A or TNF-α treated samples compared to control samples.