ArticleJournal of cellular and molecular medicine2021
Aryl hydrocarbon receptor (Ahr)-dependent Il-22 expression by type 3 innate lymphoid cells control of acute joint inflammation.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Propolis as a potential modulator of aryl hydrocarbon receptor signaling in inflammation.European cytokine network · 2026Review
- An overview of the role of the gut microbiota in rheumatoid arthritis.Microbiome research reports · 2026Review
- The Distinct Regulation of the Vitamin D and Aryl Hydrocarbon Receptors in COVID-19.Nutrients · 2024Observational
- Aryl hydrocarbon receptor: current perspectives on key signaling partners and immunoregulatory role in inflammatory diseases.Frontiers in immunology · 2024Review
- Regulation ofFrontiers in immunology · 2024Article
- Importance of crosstalk between the microbiota and the neuroimmune system for tissue homeostasis.Clinical & translational immunology · 2022Review
- Diagnostic Value of Serum Levels of IL-22, IL-23, and IL-17 for Idiopathic Pulmonary Fibrosis Associated with Lung Cancer.Therapeutics and clinical risk management · 2022Article
- Aryl hydrocarbon receptor (Ahr)-dependent Il-22 expression by type 3 innate lymphoid cells control of acute joint inflammation.Journal of cellular and molecular medicine · 2021Article
- The Aryl Hydrocarbon Receptor Suppresses Chronic Smoke-Induced Pulmonary Inflammation.Frontiers in toxicology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aryl hydrocarbon receptor (AHR) controls several inflammatory and metabolic pathways involved in various diseases, including the development of arthritis. Here, we investigated the role of AHR activation in IL-22-dependent acute arthritis using the K/BxN serum transfer model. We observed an overall reduction of cytokine expression in Ahr-deficient mice, along with decreased signs of joint inflammation. Conversely, we report worsened arthritis symptoms in Il-22 deficient mice. Pharmacological stimulation of AHR with the agonist VAG539, as well as injection of recombinant IL-22, given prior arthritogenic triggering, attenuated inflammation and reduced joint destruction. The protective effect of VAG539 was abrogated in Il-22 deficient mice. Finally, conditional Ahr depletion of Rorc-expressing cells was sufficient to attenuate arthritis, thereby uncovering a previously unsuspected role of AHR in type 3 innate lymphoid cells during acute arthritis.
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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.