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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
