ReviewWorld journal of gastrointestinal pathophysiology2016
Mechanisms of interleukin-22's beneficial effects in acute pancreatitis.
Review in World journal of gastrointestinal pathophysiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 37 citations in OpenAlex.
- Increased circulating Th22 cells in patients with acute gouty arthritis: A CONSORT-compliant article.Medicine · 2017Trial
- IL-22Rα1 restrains pancreatic injury independently of its C-terminal STAT3-amplifying domain.Journal of cell communication and signaling · 2026Article
- The role of Interleukin-22 in severe acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2024Review
- Impacts of pancreatic exocrine insufficiency on gut microbiota.Journal of Zhejiang University. Science. B · 2024Article
- Interleukin‑22 alleviates arginine‑induced pancreatic acinar cell injury via the regulation of intracellular vesicle transport system: Evidence from proteomic analysis.Experimental and therapeutic medicine · 2023Article
- Activation of the aryl hydrocarbon receptor inhibits the development of experimental autoimmune pancreatitis through IL-22-mediated signaling pathways.Clinical and experimental immunology · 2023Article
- Mt10-CVB3 Vaccine Virus Protects against CVB4 Infection by Inducing Cross-Reactive, Antigen-Specific Immune Responses.Microorganisms · 2021Article
- Article
- The role of IL22 polymorphisms on liver cirrhosis in patients with hepatitis B virus: A case control study.Medicine · 2019Article
- Detection of Reg3γ by Immunohistochemistry in Cerulein-Induced Model of Acute Pancreatic Injury in Mice and Rats.Pancreas · 2019Article
- Propolis Modulates Inflammatory Mediators and Improves Histopathology in Male Rats with L-arginine-induced Acute Pancreatitis.Sultan Qaboos University medical journal · 2019Article
- Targeting IL-10 Family Cytokines for the Treatment of Human Diseases.Cold Spring Harbor perspectives in biology · 2019Review
- Does the Automatic Measurement of Interleukin 6 Allow for Prediction of Complications during the First 48 h of Acute Pancreatitis?International journal of molecular sciences · 2018Observational
- The role of IL-22 in the resolution of sterile and nonsterile inflammation.Clinical & translational immunology · 2018Review
- Network analysis reveals crosstalk between autophagy genes and disease genes.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute pancreatitis (AP) is a disorder characterized by parenchymal injury of the pancreas controlled by immune cell-mediated inflammation. AP remains a significant challenge in the clinic due to a lack of specific and effective treatment. Knowledge of the complex mechanisms that regulate the inflammatory response in AP is needed for the development of new approaches to treatment, since immune cell-derived inflammatory cytokines have been recognized to play critical roles in the pathogenesis of the disease. Recent studies have shown that interleukin (IL)-22, a cytokine secreted by leukocytes, when applied in the severe animal models of AP, protects against the inflammation-mediated acinar injury. In contrast, in a mild AP model, endogenous IL-22 has been found to be a predominantly anti-inflammatory mediator that inhibits inflammatory cell infiltration via the induction of Reg3 proteins in acinar cells, but does not protect against acinar injury in the early stage of AP. However, constitutively over-expressed IL-22 can prevent the initial acinar injury caused by excessive autophagy through the induction of the anti-autophagic proteins Bcl-2 and Bcl-XL. Thus IL-22 plays different roles in AP depending on the severity of the AP model. This review focuses on these recently reported findings for the purpose of better understanding IL-22's regulatory roles in AP which could help to develop a novel therapeutic strategy.
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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.