ArticleJournal of autoimmunity2016
AAV-IL-22 modifies liver chemokine activity and ameliorates portal inflammation in murine autoimmune cholangitis.
Article in Journal of autoimmunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 39 citations in OpenAlex.
- Functional investigation and two-sample Mendelian randomization study of primary biliary cholangitis hub genes.World journal of clinical cases · 2024Article
- The role of Interleukin-22 in severe acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2024Review
- The effects of low-dose IL-2 on Th17/Treg cell imbalance in primary biliary cholangitis mouse models.BMC gastroenterology · 2024Article
- Regulatory T cells in inflamed liver are dysfunctional in murine primary biliary cholangitis.Clinical and experimental immunology · 2024Article
- IL-21, not IL-17A, exacerbates murine primary biliary cholangitis.Clinical and experimental immunology · 2024Article
- Animal models of primary biliary cholangitis: status and challenges.Cell & bioscience · 2023Review
- Apoptotic biliary epithelial cells and gut dysbiosis in the induction of murine primary biliary cholangitis.Journal of translational autoimmunity · 2023Article
- Interleukin-30 Suppresses Not Only CD4Biomedicines · 2021Article
- A Double Edged Sword Role of Interleukin-22 in Wound Healing and Tissue Regeneration.Frontiers in immunology · 2020Review
- Pathogen infections and primary biliary cholangitis.Clinical and experimental immunology · 2019Review
- Endogenous IL-10 maintains immune tolerance but IL-10 gene transfer exacerbates autoimmune cholangitis.Journal of autoimmunity · 2018Article
- Proteomic analysis reveals distinctive protein profiles involved in CD8Cellular & molecular immunology · 2018Article
- Therapeutic and immunological interventions in primary biliary cholangitis: from mouse models to humans.Archives of medical science : AMS · 2018Article
- The Therapeutic Potential and Molecular Mechanism of Isoflavone Extract against Psoriasis.Scientific reports · 2018Article
- The interplay of type I and type II interferons in murine autoimmune cholangitis as a basis for sex-biased autoimmunity.Hepatology (Baltimore, Md.) · 2018Article
- Myeloid Cells and Chronic Liver Disease: a Comprehensive Review.Clinical reviews in allergy & immunology · 2018Review
- A Mouse Model of Autoimmune Cholangitis via Syngeneic Bile Duct Protein Immunization.Scientific reports · 2017Article
- Primary biliary cholangitis: a comprehensive overview.Hepatology international · 2017Review
- Geoepidemiology and changing mortality in primary biliary cholangitis.Journal of gastroenterology · 2017Review
- The fingerprint of antimitochondrial antibodies and the etiology of primary biliary cholangitis.Hepatology (Baltimore, Md.) · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
There remain significant obstacles in developing biologics to treat primary biliary cholangitis (PBC). Although a number of agents have been studied both in murine models and human patients, the results have been relatively disappointing. IL-22 is a member of the IL-10 family and has multiple theoretical reasons for predicting successful usage in PBC. We have taken advantage of an IL-22 expressing adeno-associated virus (AAV-IL-22) to address the potential role of IL-22 in not only protecting mice from autoimmune cholangitis, but also in treating animals with established portal inflammation. Using our established mouse model of 2-OA-OVA immunization, including α-galactosylceramide (α-GalCer) stimulation, we treated mice both before and after the onset of clinical disease with AAV-IL-22. Firstly, AAV-IL-22 treatment given prior to 2-OA-OVA and α-GalCer exposure, i.e. before the onset of disease, significantly reduces the portal inflammatory response, production of Th1 cytokines and appearance of liver fibrosis. It also reduced the liver lymphotropic chemokines CCL5, CCL19, CXCL9, and CXCL10. Secondly, and more importantly, therapeutic use of AAV-IL-22, administered after the onset of disease, achieved a greater hurdle and significantly improved portal pathology. Further the improvements in inflammation were negatively correlated with levels of CCL5 and CXCL10 and positively correlated with levels of IL-22. In conclusion, we submit that the clinical use of IL-22 has a potential role in modulating the inflammatory portal process in patients with PBC.
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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.