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The pathophysiological mechanisms of migraine remain controversial. Recent studies have suggested that immune dysfunction may be involved in the pathogenesis of migraine. The AHR, a receptor expressed on most immune cells, has been implicated in the occurrence of many autoimmune diseases; however, whether it is involved in the pathogenesis of migraine is unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A chronic migraine rat model was established through repeated intraperitoneal injection of nitroglycerin (NTG). The mechanical and thermal pain thresholds were assessed using von Frey filaments and radiant heat. Next, the protein expression levels of AHR in the trigeminal nucleus caudalis (TNC) region of chronic migraine (CM)\u2010like rats were quantified and the changes in Treg\/Th17\u2010related transcription factors and inflammatory factors in the TNC were explored. To determine the role of AHR in CM, we examined the effects of the AHR agonist 2\u2010(1\u2032\u2010indole\u20103\u2032\u2010carbonyl)\u2010thiazole\u20104\u2010carboxylic acid methyl ester (ITE), and AHR antagonist CH\u2010223191 on pain behavior, c\u2010Fos, calcitonin gene\u2010related peptide (CGRP), AHR, and Treg\/Th17\u2010related factor expression in CM\u2010like rats.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Repeated administration of NTG significantly enhanced nociceptive hypersensitivity and increased expression of c\u2010Fos and CGRP in rats, while AHR was significantly decreased in the TNC. In addition, the expression of the transcription factor forkhead box protein P3 and the signal transducer and activator of transcription 5 decreased significantly. In contrast, the expression of the transcription factor retinoic acid receptor\u2010related orphan receptor \u03b3 t and signal transducer and activator of transcription 3 were significantly increased. Moreover, the mRNA level of transforming growth factor beta\u20101 was decreased, while that of interleukin (IL)\u201010 and IL\u201022 was increased in the TNC. The AHR agonist ITE alleviated migraine\u2010like pain behaviors in rats, activated the AHR signaling pathway, and improved the imbalance of Treg\/Th17\u2010related transcription factors and inflammatory factors. Conversely, the AHR antagonist CH\u2010223191 did not alleviate migraine\u2010like pain behaviors in rats; and even exacerbated them.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The AHR participates in the development of CM by regulating Treg\/Th17\u2010related homeostasis. Therefore, treatments targeting the AHR\/Treg\/Th17 signaling pathway could be new effective interventions for CM treatment.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/head.14599","type":"journal-article","created":{"date-parts":[[2023,8,4]],"date-time":"2023-08-04T07:31:08Z","timestamp":1691134268000},"page":"1045-1060","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Aryl hydrocarbon receptors improve migraine\u2010like pain behaviors in rats through the regulation of regulatory T cell\/T\u2010helper 17 cell\u2010related homeostasis"],"prefix":"10.1111","volume":"63","author":[{"given":"Liu","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Neurology Renmin Hospital of Wuhan University, Wuhan University  Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanjie","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Neurology 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