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. 2016 Oct 27;15:67. doi: 10.1186/s12943-016-0551-1

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© The Author(s). 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 5 — The IL-17 F signaling pathway is epigenetically altered in malignant COPD and non-malignant COPD lung airway epithelial cells. Top disrupted downstream molecular components of the IL-17 F pathway are involved in mediating inflammatory and anti-microbial processes. Genes involved in IL-17A signaling pathways and that overlap with deregulations in the IL-17 F signaling pathway are also depicted. CCL2: chemokine (C-C motif) ligand 2; CXCL1: chemokine (C-X-C motif) ligand 1; G-CSF: granulocyte colony-stimulating factor 3; CX3CL1: chemokine (C-X3-C motif) ligand 1, GM-CSF: granulocyte-macrophage colony-stimulating factor; HBD1: defensin beta 1; IL: interleukin; IL-17RA: interleukin 17 receptor A; IL- 17RC: interleukin 17 receptor C; LCN2: lipocalin 2