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. 2019 Jan 17;3(3):392–405. doi: 10.1002/hep4.1303

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© 2019 The Authors. Hepatology Communications published by Wiley Periodicals, Inc., on behalf of the American Association for the Study of Liver Diseases.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Effect of IL‐22BP on IL‐22‐induced production of proinflammatory mediators and cell viability. (A) Cell viability was assessed in Huh‐7 cells using the WST‐1 assay 6 hours after stimulation with IL‐22 with or without IL‐22BP at the indicated concentrations. (B) Induction of TNF‐α mRNA in Huh‐7.5 cells treated for 6 hours with the indicated concentrations of IL‐22. TNF‐α mRNA levels were quantified by quantitative polymerase chain reaction (PCR) and expressed relative to GAPDH (glyceraldehyde 3‐phosphate dehydrogenase). (C) Huh‐7 cells and HepG2 cells were stimulated with IL‐22 with or without IL‐22BP at the indicated concentrations for 6 hours. mRNA levels of LBP were quantified by quantitative PCR and expressed relative to GAPDH. (D) Quantification of LBP protein levels in HepG2 cells stimulated with IL‐22 for the indicated time points. (E) IL‐22BP abolishes IL‐22‐mediated LBP protein production in HepG2 cells and primary human hepatocytes. Cells were stimulated with 5 ng/mL of IL‐22 and ascending concentrations of IL‐22BP for 24 hours. Protein levels were analyzed by immunoblotting using β‐actin as a control.