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Updated: Jul 11, 2026

Visualization of IL-22-expressing Lymphocytes Using Reporter Mice
Published on: January 25, 2017
Interleukin-22 but not interleukin-17 provides protection to hepatocytes during acute liver inflammation
Lauren A Zenewicz1, George D Yancopoulos, David M Valenzuela
1Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Abstract:
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.
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