The double-edged role of IL-22 in organ fibrosis

Immunopharmacol Immunotoxicol. 2020 Oct;42(5):392-399. doi: 10.1080/08923973.2020.1799388. Epub 2020 Aug 4.

Abstract

Fibrosis is unregulated tissue repair in damaged or diseased organs, and the accumulation of excess extracellular matrix (ECM) impacts the structure and functions of organs, leading to death. Fibrosis is usually triggered by inflammation and tissue damage, and inflammatory mediators stimulate the proliferation of myofibroblasts and the excessive production of ECM. The IL-10 family cytokines play important roles in the development of fibrosis, and its member IL-22 has recently attracted specific attention. IL-22 plays great roles in preventing pathogens invasion and tissue damage, as well as making a contribution to pathogenic processes. Increasing evidence suggested that IL-22 is a key molecule in tissue repair, proliferation and mucosal barrier defense, and it has also been suggested to play both pro-fibrotic and anti-fibrotic roles in tissues. In this review, we summarized the pro-fibrotic and anti-fibrotic functions of IL-22 in various organs which may be of great significance for the development of potential therapeutic strategies for fibrosis-related diseases.

Keywords: IL-22; dual role; fibrosis; inflammation; repair.

Publication types

  • Review

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / therapeutic use
  • Extracellular Matrix / drug effects
  • Extracellular Matrix / metabolism*
  • Extracellular Matrix / pathology
  • Fibrosis
  • Humans
  • Inflammation / drug therapy
  • Inflammation / metabolism*
  • Inflammation / pathology
  • Interleukin-22
  • Interleukins / metabolism*
  • Interleukins / therapeutic use
  • Myofibroblasts / drug effects
  • Myofibroblasts / metabolism*
  • Myofibroblasts / pathology
  • Signal Transduction

Substances

  • Anti-Inflammatory Agents
  • Interleukins