Journal
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
Volume 25, Issue 10, Pages 4721-4731Publisher
WILEY
DOI: 10.1111/jcmm.16433
Keywords
acute arthritis; aryl hydrocarbon receptor; IL‐ 22; inflammation
Categories
Funding
- le Centre National de la Recherche Scientifique (CNRS)
- European Regional Development Fund (FEDER) [N 2016-00110366, EX005756]
- Agence Nationale de la Recherche (ANR) [ANR-11-LABX-0070_TRANSPLANTEX]
- Institut National de la Sante et de la Recherche Medicale (INSERM)
- Institut Universitaire de France (IUF)
- MSD-Avenir grant AUTOGEN
- University of Strasbourg (including IDEX UNISTRA)
- European regional development fund (European Union) INTERREG V programs
- Federation Hospitalo-Universitaire (FHU) OMICARE
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The study revealed the crucial role of AHR activation in the development of arthritis, while IL-22 deficiency aggravated arthritis symptoms. Activation of AHR can alleviate inflammation and reduce joint destruction, with a protective effect on type 3 innate lymphoid cells during acute arthritis.
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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