ArticleGastroenterology2012
Interleukin-22 promotes proliferation of liver stem/progenitor cells in mice and patients with chronic hepatitis B virus infection.
Article in Gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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Who cites it
89 citing papers in PubMed, 156 citations in OpenAlex.
- Bayesian analysis of cytokines and chemokine identifies immune pathways of HBsAg loss during chronic hepatitis B treatment.Scientific reports · 2021Trial
- An Update on IL-22 Therapies in Alcohol-Associated Liver Disease and Beyond.The American journal of pathology · 2026Review
- The Cellular and Molecular Characteristics of Postnatal Human Thymus Stromal Stem Cells.Biomedicines · 2025Article
- Novel treatment of acute and acute-on-chronic liver failure: Interleukin-22.Liver international : official journal of the International Association for the Study of the Liver · 2025Review
- The AhR/IL-22 axis in chronic gut inflammation: unraveling mechanisms and therapeutic prospects.Frontiers in immunology · 2025Review
- Immunology and treatments of fatty liver disease.Archives of toxicology · 2025Review
- The role of the interleukin family in liver fibrosis.Frontiers in immunology · 2025Review
- Insight into the mechanisms regulating liver cancer stem cells by hepatitis B virus X protein.Infectious agents and cancer · 2024Review
- Role of HIF-1α-Activated IL-22/IL-22R1/Bmi1 Signaling Modulates the Self-Renewal of Cardiac Stem Cells in Acute Myocardial Ischemia.Stem cell reviews and reports · 2024Article
- Review of the potential value of serum interleukin levels as prognostic biomarkers of liver failure.World journal of clinical cases · 2024Review
- The roles of Th cells in myocardial infarction.Cell death discovery · 2024Review
- GITRL impairs hepatocyte repopulation by liver progenitor cells to aggravate inflammation and fibrosis by GITRCell death & disease · 2024Article
- Role of the type 3 cytokines IL-17 and IL-22 in modulating metabolic dysfunction-associated steatotic liver disease.Frontiers in immunology · 2024Review
- The Role of Interleukins in HBV Infection: A Narrative Review.Journal of personalized medicine · 2023Review
- The role of CD4MedComm · 2023Review
- Article
- Risk factors of primary liver cancer initiation associated with tumour initiating cell emergence: novel targets for promising preventive therapies.eGastroenterology · 2023Review
- Current Knowledge of Th22 Cell and IL-22 Functions in Infectious Diseases.Pathogens (Basel, Switzerland) · 2023Review
- GITR/GITRL reverse signalling modulates the proliferation of hepatic progenitor cells by recruiting ANXA2 to phosphorylate ERK1/2 and Akt.Cell death & disease · 2022Article
- Serum Interleukins as Potential Prognostic Biomarkers in HBV-Related Acute-on-Chronic Liver Failure.Mediators of inflammation · 2022Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsProliferation of liver stem/progenitor cells (LPCs), which can differentiate into hepatocytes or biliary epithelial cells, is often observed in chronically inflamed regions of liver in patients. We investigated how inflammation might promote proliferation of LPCs.
methodsWe examined the role of interleukin (IL)-22, a survival factor for hepatocytes, on proliferation of LPCs in patients with chronic hepatitis B virus (HBV) infection and in mice. Proliferation of LPCs in mice was induced by feeding a diet that contained 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC).
resultsHepatic expression of IL-22 was increased in patients with HBV and correlated with the grade of inflammation and proliferation of LPCs. Mice on the DDC diet that overexpressed an IL-22 transgene specifically in liver (IL-22TG), or that were infected with an IL-22-expressing adenovirus, had increased proliferation of LPCs. Signal transducer and activator of transcription (STAT) 3, a component of the IL-22 signaling pathway, was activated in LPCs isolated from DDC-fed IL-22TG mice. Deletion of STAT3 from livers of IL-22TG mice reduced proliferation of LPCs. In addition, the receptors IL-22R1 and IL-10R2 were detected on epithelial cell adhesion molecule(+)CD45(-) LPCs isolated from DDC-fed wild-type mice. Culture of these cells with IL-22 activated STAT3 and led to cell proliferation, but IL-22 had no effect on proliferation of STAT3-deficient EpCAM(+)CD45(-) LPCs. IL-22 also activated STAT3 and promoted proliferation of cultured BMOL cells (a mouse LPC line).
conclusionsIn livers of mice and patients with chronic HBV infection, inflammatory cells produce IL-22, which promotes proliferation of LPCs via STAT3. These findings link inflammation with proliferation of LPCs in patients with HBV infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.