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芳烃受体（Ahr）依赖的3型天然淋巴细胞表达白细胞介素-22对急性关节炎症的控制

Aryl hydrocarbon receptor (Ahr)-dependent Il-22 expression by type 3 innate lymphoid cells control of acute joint inflammation.

作者信息

Nehmar Ramzi, Fauconnier Louis, Alves-Filho Jose, Togbe Dieudonnée, DeCauwer Aurore, Bahram Seiamak, Le Bert Marc, Ryffel Bernhard, Georgel Philippe

机构信息

Laboratoire d'ImmunoRhumatologie Moléculaire, Institut national de la santé et de la recherche médicale (INSERM) UMR_S 1109, Institut thématique interdisciplinaire (ITI) de Médecine de Précision de Strasbourg, Transplantex NG, Faculté de Médecine, Fédération Hospitalo-Universitaire OMICARE, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Université de Strasbourg, Strasbourg, France.

ArtImmune SAS, Orleans, France.

出版信息

J Cell Mol Med. 2021 May;25(10):4721-4731. doi: 10.1111/jcmm.16433. Epub 2021 Mar 18.

DOI:10.1111/jcmm.16433
PMID:33734594
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8107095/
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.

摘要

芳烃受体（AHR）控制着多种疾病中涉及的几种炎症和代谢途径，包括关节炎的发展。在此，我们使用K/BxN血清转移模型研究了AHR激活在白细胞介素-22（IL-22）依赖性急性关节炎中的作用。我们观察到Ahr基因缺陷小鼠体内细胞因子表达总体下降，同时关节炎症迹象减少。相反，我们报告白细胞介素-22基因缺陷小鼠的关节炎症状加重。在致关节炎触发之前，用激动剂VAG539对AHR进行药理刺激以及注射重组白细胞介素-22，可减轻炎症并减少关节破坏。VAG539的保护作用在白细胞介素-22基因缺陷小鼠中被消除。最后，对表达Rorc的细胞进行条件性Ahr基因敲除足以减轻关节炎，从而揭示了AHR在急性关节炎期间3型天然淋巴细胞中以前未被怀疑的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/666e/8107095/a05c3fdeccc2/JCMM-25-4721-g004.jpg
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