scholarly journals The aryl hydrocarbon receptor: a regulator of Th17 and Treg cell development in disease

Cell Research ◽  
2008 ◽  
Vol 18 (6) ◽  
pp. 605-608 ◽  
Author(s):  
Peggy P Ho ◽  
Lawrence Steinman
Blood ◽  
2018 ◽  
Vol 132 (17) ◽  
pp. 1792-1804 ◽  
Author(s):  
Steven D. Scoville ◽  
Ansel P. Nalin ◽  
Luxi Chen ◽  
Li Chen ◽  
Michael H. Zhang ◽  
...  

Key Points Human and murine AML activate the AHR pathway, which can regulate miR-29b expression and impair NK cell development and function. AML-induced impairment of NK cell development and function can be reversed with AHR antagonist.


Placenta ◽  
2021 ◽  
Vol 112 ◽  
pp. e54
Author(s):  
Vinay Shukla ◽  
Khursheed Iqbal ◽  
Anna M. Galligos ◽  
Carrie A. Vyhlidal ◽  
Michael J. Soares

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e106955 ◽  
Author(s):  
Mark D. Hayes ◽  
Vitalijs Ovcinnikovs ◽  
Andrew G. Smith ◽  
Ian Kimber ◽  
Rebecca J. Dearman

Immunity ◽  
2016 ◽  
Vol 45 (1) ◽  
pp. 185-197 ◽  
Author(s):  
Shiyang Li ◽  
Jennifer J. Heller ◽  
John W. Bostick ◽  
Aileen Lee ◽  
Hilde Schjerven ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-19
Author(s):  
Chang Liu ◽  
Yanyang Li ◽  
Yanping Chen ◽  
Shaowei Huang ◽  
Xiaojing Wang ◽  
...  

As one of the ligands of aryl hydrocarbon receptor (AhR), baicalein, isolated from Scutellaria baicalensis Georgi, has been proved to exert potential therapeutic effects on ulcerative colitis (UC), but its therapeutic mechanism remains obscure. Authentically, ulcerative colitis can be alleviated by regulating the differentiation of naïve CD4+ T cells via AhR activation. So, our study planned to prove the hypothesis that baicalein protected mice against UC by regulating the balance of Th17/Treg cells via AhR activation. Immunofluorescence and western blot results showed that baicalein could promote AhR activation and induce it to transfer to the nucleus. We further determined the effect of baicalein on naïve CD4+ T cell differentiation in vitro by magnetic cell separation and drug intervention. The results showed that baicalein could promote Treg cell differentiation by activating AhR. In vivo study, UC mice were established by free drinking of dextran sulfate sodium (DSS) for 7 days and then were orally administrated by baicalein (10, 20, and 40 mg/kg), TCDD (AhR agonist), and CH223191 (antagonist). The results demonstrated that baicalein improved the symptoms of UC mice, regulated the balance of Th17/Treg cells, and restored the balance of proinflammatory cytokines such as IL-17, IL-6, and TNF-α; anti-inflammatory cytokines such as IL-10 and TGF-β; and epithelial protective cytokine IL-22 in UC mice, and these effects were related to AhR. Taken together, our research found that baicalein might be a potential drug for UC via regulating Treg cell differentiation and maintaining immune homeostasis and attempted to shed a light on the pivotal role of AhR in these effects.


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