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Journal of Immunology Research
Volume 2016, Article ID 2148129, 8 pages
Review Article

How Does Interleukin-22 Mediate Liver Regeneration and Prevent Injury and Fibrosis?

1Cell & Molecular Biology Lab, Department of Zoology, University of the Punjab, Lahore, Pakistan
2Centennial College, Scarborough, Toronto, ON, Canada

Received 29 August 2016; Revised 13 October 2016; Accepted 25 October 2016

Academic Editor: Ethan M. Shevach

Copyright © 2016 Muhammad Babar Khawar et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Interleukin-22 (IL-22) is a pluripotent T cell-derived cytokine which is a member of IL-10 cytokine family. It is the only interleukin produced by immune cells but does not target immune system components. IL-22 is mainly produced by dendritic cells (DCs) and TH17, TH22, NK, and NKT cells and targets a number of body tissues including liver, pancreas, and other epithelial tissues. It provokes a series of downstream signaling pathways upon binding with IL-22R complex which protects liver damage through STAT3 activation. IL-22BP is an inhibitor of IL-22 which has 20–1000x more affinity to bind with IL-22 compared to IL-22R1 that inhibits IL-22 activity. Its level was found to be positively correlated with the severity of liver damage and fibrosis. So, the present review is an effort to reveal the exact mechanism lying in the hepatoprotective activity of IL-22 and some of its future therapeutic implications.