The role of interleukin-22 in hepatitis C virus infection

Dambacher, Julia; Beigel, Florian; Zitzmann, Kathrin; Heeg, Malte; Göke, Burkhard; Diepolder, Helmut M.; Auernhammer, Christoph J.; Brand, Stephan

doi:10.1016/j.cyto.2007.11.016

Cited by 81 publications

(75 citation statements)

References 38 publications

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“…These data are in line with other studies reporting no direct or indirect antiviral activity of IL-22 (45)(46)(47)(48)(49). Furthermore, in agreement with a previous finding showing that IL-22 has no impact on Ag-driven lymphocyte priming and expansion (65), Il22 Ϫ/Ϫ mice had a normal IAV-specific CD8 ϩ T cell response.…”

Section: Discussionsupporting

confidence: 82%

“…Recent data also indicated that reduced IL-22 production in the gut mucosa is important in human immunodeficiency virus mucosal immunopathogenesis (44). On the other hand, although hepatic IL-22 expression is upregulated in viral hepatitis, IL-22 lacks direct antiviral activity against hepatitis B and C viruses (45,46). Of interest, IL-22 aggravates tissue inflammation during experimental hepatitis B virus infection (47) and West Nile virus encephalitis (48).…”

mentioning

confidence: 99%

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Interleukin-22 Reduces Lung Inflammation during Influenza A Virus Infection and Protects against Secondary Bacterial Infection

Ivanov

Renneson

Fontaine

et al. 2013

J Virol

135

146

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Section: Discussionsupporting

confidence: 82%

mentioning

confidence: 99%

Interleukin-22 Reduces Lung Inflammation during Influenza A Virus Infection and Protects against Secondary Bacterial Infection

Ivanov

Renneson

Fontaine

et al. 2013

J Virol

135

146

View full text Add to dashboard Cite

“…Moreover, our finding indicates that IL-22 plays a positive role in the control of epithelial damage early after IAV infection. On the other hand, IL-22 lacks direct antiviral activity against IAV both in vitro and in vivo, as recently shown for hepatitis B and C viruses (91,92). These data are in contrast with those from Guo and Topham (88), who suggested that IL-22 rather favors viral replication by sustaining epithelial cells.…”

Section: Discussioncontrasting

confidence: 56%

Interleukin-22 Is Produced by Invariant Natural Killer T Lymphocytes during Influenza A Virus Infection

Paget

Ivanov

Fontaine

et al. 2012

Journal of Biological Chemistry

159

167

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Background: Invariant natural killer T (iNKT) cells play a beneficial role during experimental influenza A virus (IAV) infection.Results: iNKT cells produce IL-22 during infection, and IL-22 prevents the IAV-triggered cell death of pulmonary epithelium. Conclusion: IL-22 produced by iNKT cells might be important during IAV infection.Significance: Understanding how iNKT cells function during IAV infection might be instrumental to control IAV-associated pathogenesis.

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“…Protective effects of IL-22 in the context of hepatitis were subsequently confirmed by Zenewicz et al (26) using IL-22-deficient mice. Brand et al (39) proposed that IL-22 is able to maintain metabolic activity of primary human hepatocytes in vitro with IL-22 transcription induced in the liver in the context of human hepatitis (46). Ren et al (40) have most recently shown that IL-22 plays a role in liver regeneration subsequent to partial hepatectomy.…”

Section: Discussionmentioning

confidence: 99%

IL-22 Induces an Acute-Phase Response

Liang

Nickerson‐Nutter

Pittman

et al. 2010

The Journal of Immunology

167

146

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IL-22 is made by a unique set of innate and adaptive immune cells, including the recently identified noncytolytic NK, lymphoid tissue-inducer, Th17, and Th22 cells. The direct effects of IL-22 are restricted to nonhematopoietic cells, its receptor expressed on the surface of only epithelial cells and some fibroblasts in various organs, including parenchymal tissue of the gut, lung, skin, and liver. Despite this cellular restriction on IL-22 activity, we demonstrate that IL-22 induces effects on systemic biochemical, cellular, and physiological parameters. By utilizing adenoviral-mediated delivery of IL-22 and systemic administration of IL-22 protein, we observed that IL-22 modulates factors involved in coagulation, including fibrinogen levels and platelet numbers, and cellular constituents of blood, such as neutrophil and RBC counts. Furthermore, we observed that IL-22 induces thymic atrophy, body weight loss, and renal proximal tubule metabolic activity. These cellular and physiological parameters are indicative of a systemic inflammatory state. We observed that IL-22 induces biochemical changes in the liver including induction of fibrinogen, CXCL1, and serum amyloid A that likely contribute to the reported cellular and physiological effects of IL-22. Based on these findings, we propose that downstream of its expression and impact in local tissue inflammation, circulating IL-22 can further induce changes in systemic physiology that is indicative of an acute-phase response.

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The role of interleukin-22 in hepatitis C virus infection

Cited by 81 publications

References 38 publications

Interleukin-22 Reduces Lung Inflammation during Influenza A Virus Infection and Protects against Secondary Bacterial Infection

Interleukin-22 Reduces Lung Inflammation during Influenza A Virus Infection and Protects against Secondary Bacterial Infection

Interleukin-22 Is Produced by Invariant Natural Killer T Lymphocytes during Influenza A Virus Infection

IL-22 Induces an Acute-Phase Response

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