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Interleukin-22 but not interleukin-17 provides protection to hepatocytes during acute liver inflammation.

The cytokine interleukin-22 (IL-22) is primarily expressed by T helper 17 (Th17) CD4(+) T cells and is highly upregulated during chronic inflammatory diseases. IL-22 receptor expression is absent on immune cells, but is instead restricted to the tissues, providing signaling directionality from the immune system to the tissues. However, the role of IL-22 in inflammatory responses has been confounded by data suggesting both pro- and anti-inflammatory functions. Herein, we provide evidence that during inflammation, IL-22 played a protective role in preventing tissue injury. Hepatocytes from mice deficient in IL-22 were highly sensitive to the detrimental immune response associated with hepatitis. Additionally, IL-22-expressing Th17 cells provided protection during hepatitis in IL-22-deficient mice. On the other hand, interleukin-17 (IL-17), which is coexpressed with IL-22 and can induce similar cellular responses, had no observable role in liver inflammation. Our data suggest that IL-22 serves as a protective molecule to counteract the destructive nature of the immune response to limit tissue damage.

Pubmed ID: 17919941


  • Zenewicz LA
  • Yancopoulos GD
  • Valenzuela DM
  • Murphy AJ
  • Karow M
  • Flavell RA



Publication Data

October 30, 2007

Associated Grants

  • Agency: NIAID NIH HHS, Id: 2-T32-AI07019-29
  • Agency: NIAID NIH HHS, Id: T32 AI007019
  • Agency: NIAID NIH HHS, Id: T32 AI007019-29
  • Agency: Howard Hughes Medical Institute, Id:

Mesh Terms

  • Adoptive Transfer
  • Animals
  • CD4-Positive T-Lymphocytes
  • Enzyme-Linked Immunosorbent Assay
  • Flow Cytometry
  • Hepatitis
  • Hepatocytes
  • Interleukin-17
  • Interleukin-6
  • Interleukins
  • Mice
  • RNA, Messenger
  • Reverse Transcriptase Polymerase Chain Reaction
  • T-Lymphocyte Subsets