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. 2020 Apr 10;18(4):379–401. doi: 10.5217/ir.2019.09148

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© Copyright 2020. Korean Association for the Study of Intestinal Diseases. All rights reserved.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 1. — Pathophysiological process to fibrotic strictures. APCs, antigen presenting cells; ILs, interleukins; Th0, naïve T cells; Th, T helper cells; IFN-γ, interferon-γ; TNF-α, tumor necrosis factor α; ROS, reactive oxygen species; TGF-β1, transforming growth factor-β1; CTGF, connective tissue growth factor; PDGF, platelet-derived growth factor; FGF, fibroblast growth factor; IGF, insulin-like growth factor; MMP9, matrix metalloproteinase 9; SMCs, smooth muscle cells; SEMFs, subepithelial myofibroblasts; ICC, interstitial cells of Cajal; EMT, epithelial mesenchymal transition; Endo-MT, endothelial mesenchymal transition; BM-MSCs, bone marrow derived mesenchymal stem cells; ECM, extracellular matrix.