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. 2020 Jan 28;69(9):1677–1690. doi: 10.1136/gutjnl-2019-319091

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© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Infiltration of immune cells into the liver tissue of AON-treated MDR2-KO mice compared with controls. An anti-inflammatory role of TGF-β2 was suggested. (A) In AON-treated MDR2-KO mice, increased amounts of resident F4/80-positive macrophages were detected. These are probably not polarised to typical M1 or M2 phenotypes as levels of (B) TnfA, Il6 and Il1B and (C) Il13, Il4 and Arg1 were not changed by AON treatment. (D) Immunohistochemical staining of CD45 revealed significant downregulation in AON-treated MDR2-KO mice. *p≤0.05, **p≤0.01, ***p≤0.001. Scale bars indicate (A) 50 µm or (D) 200 µm. AON, antisense oligonucleotides; Arg, arginase; Il, interleucin; MDR2-KO, multidrug resistance gene 2 knockout; TGFB, transforming growth factor beta; Tnfa, tumour necrosis factor-alpha.