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. 2009 Jul 6;206(7):1457–1464. doi: 10.1084/jem.20090207

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© 2009 Wang et al.

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Figure 4. — IL-17 activates Stat3 in tumor and tumor stromal cells through an IL-6–dependent mechanism. (A) The kinetics of Stat3 activation in B16 melanoma cells, MEFs, endothelial cells (ECP), splenic CD11c⁺ DCs, or splenic CD11b⁺ myeloid cells after stimulation with recombinant IL-17. Western blots of phospho-Stat3, total Stat3, and β-actin are shown and are representative of two independent experiments. (B and C) IL-17 induces IL-6 expression in tumor and various tumor stromal cells. (B) IL-6 levels in B16 cells treated for 24 h with recombinant IL-17 were assessed by quantitative real-time PCR (left) and ELISA (second from left). IL-6 induction in MB49 tumor cells (middle), MEFs (second from right), and endothelial cells (ECP; right) by recombinant IL-17 treatment is shown (from three independent experiments; P < 0.0001). Data represent means ± SEM. (C) Production of IL-6 by CD11c⁺ DCs upon IL-17 stimulation, as determined by ELISA (from three independent experiments; P = 0.0002). Data represent means ± SEM. (D) IL-17–induced Stat3 activation is IL-6 dependent. (top) MB49 tumor cells were incubated with IL-17 with or without anti–IL-6 or –IL-10 antibodies, and Western blots were performed for phospho-Stat3, total Stat3, and β-actin protein levels. (bottom) MEFs and splenic CD11c⁺ DCs were stimulated with IL-17 in the presence of IL-6–neutralizing antibodies or control IgG (representative of three independent experiments).