scholarly journals The Aryl Hydrocarbon Receptor Preferentially Marks and Promotes Gut Regulatory T Cells

Cell Reports ◽  
2017 ◽  
Vol 21 (8) ◽  
pp. 2277-2290 ◽  
Author(s):  
Jian Ye ◽  
Ju Qiu ◽  
John W. Bostick ◽  
Aki Ueda ◽  
Hilde Schjerven ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Aryl Hydrocarbon Receptor ◽  
Aryl Hydrocarbon

Dietary Flavonoid Naringenin Induces Regulatory T Cells via an Aryl Hydrocarbon Receptor Mediated Pathway

2012 ◽  
Vol 60 (9) ◽  
pp. 2171-2178 ◽  
Author(s):  
Hsi-Kai Wang ◽  
Chen-Hao Yeh ◽  
Taku Iwamoto ◽  
Hideo Satsu ◽  
Makoto Shimizu ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Aryl Hydrocarbon Receptor ◽  
Aryl Hydrocarbon ◽  
Dietary Flavonoid

scholarly journals The aryl hydrocarbon receptor interacts with c-Maf to promote the differentiation of type 1 regulatory T cells induced by IL-27

2010 ◽  
Vol 11 (9) ◽  
pp. 854-861 ◽  
Author(s):  
Lionel Apetoh ◽  
Francisco J Quintana ◽  
Caroline Pot ◽  
Nicole Joller ◽  
Sheng Xiao ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Aryl Hydrocarbon Receptor ◽  
Aryl Hydrocarbon

5-Aminosalicylic Acid, A Weak Agonist for Aryl Hydrocarbon Receptor That Induces Splenic Regulatory T Cells

Pharmacology ◽  
2021 ◽  
pp. 1-7
Author(s):  
Atsuhito Kubota ◽  
Masaru Terasaki ◽  
Rie Takai ◽  
Masaki Kobayashi ◽  
Ryuta Muromoto ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Aryl Hydrocarbon Receptor ◽  
Flow Cytometry Analysis ◽  
Aminosalicylic Acid ◽  
Aryl Hydrocarbon ◽  
Transactivation Assay ◽  
Splenic Cells ◽  
Inflammatory Bowel

<b><i>Introduction:</i></b> 5-Aminosalicylic acid (5-ASA) is widely used as a key drug in inflammatory bowel disease. It has been recently reported that 5-ASA induces CD4 + Foxp3 + regulatory T cells (Tregs) in the colon via the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor that regulates inflammation. However, the role of 5-ASA as an AhR agonist that induces Tregs in the spleen remains unknown. <b><i>Methods:</i></b> In the present study, we investigated these themes using an AhR-mediated transactivation assay and flow cytometry analysis. The experiments were conducted by using DR-EcoScreen cells and C57BL/6 mice. <b><i>Results:</i></b> The DR-EcoScreen cell-based transactivation assay revealed that 5-ASA acted as a weak AhR agonist at concentrations of ≥300 μM (1.31–1.45-fold), and that a typical AhR agonist, 2,3,7,8-tetrachlorodibenzo-<i>p</i>-dioxin (TCDD), activated AhR at a concentration of 0.1 nM (22.8-fold). In addition, the treatment of mouse splenic cells with 300 μM 5-ASA in a primary culture assay significantly induced CD4+CD25 + Foxp3 + Tregs (control vs. 5-ASA: 9.0% vs. 12.65%, <i>p</i> &#x3c; 0.05), while 0.1 nM TCDD also showed significant induction of Tregs (control vs. TCDD: 9.0% vs. 14.1%, <i>p</i> &#x3c; 0.05). Interestingly, this induction was eliminated by co-treatment with an AhR antagonist, CH-223191. <b><i>Discussion:</i></b> These results suggest that 5-ASA is a weak agonist of AhR and thereby induces Tregs in spleen cells. Our findings may provide useful insights into the mechanism by which 5-ASA regulates inflammation.

Activation of the aryl hydrocarbon receptor reduces the number of precursor and effector T cells, but preserves thymic CD4+CD25+Foxp3+ regulatory T cells

2012 ◽  
Vol 215 (2) ◽  
pp. 100-109 ◽  
Author(s):  
V.J. Schulz ◽  
J.J. Smit ◽  
M. Bol-Schoenmakers ◽  
M.B.M. van Duursen ◽  
M. van den Berg ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Aryl Hydrocarbon Receptor ◽  
Effector T Cells ◽  
Aryl Hydrocarbon

scholarly journals Induction of Colonic Regulatory T Cells by Mesalamine by Activating the Aryl Hydrocarbon Receptor

2017 ◽  
Vol 4 (1) ◽  
pp. 135-151 ◽  
Author(s):  
Kyoko Oh-oka ◽  
Yuko Kojima ◽  
Koichiro Uchida ◽  
Kimiko Yoda ◽  
Kayoko Ishimaru ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Aryl Hydrocarbon Receptor ◽  
Aryl Hydrocarbon

scholarly journals An endogenous aryl hydrocarbon receptor ligand, ITE, induces regulatory T cells and ameliorates experimental colitis

2018 ◽  
Vol 315 (2) ◽  
pp. G220-G230 ◽  
Author(s):  
Jessica D. Abron ◽  
Narendra P. Singh ◽  
Manoj K. Mishra ◽  
Robert L. Price ◽  
Mitzi Nagarkatti ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
Methyl Ester ◽  
Regulatory T Cells ◽  
Aryl Hydrocarbon Receptor ◽  
Inflammatory Cytokines ◽  
Acid Methyl Ester ◽  
Aryl Hydrocarbon ◽  
Acid Methyl ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) is a chronic intestinal inflammatory condition that affects millions of people with high morbidity and health care costs. The precise etiology of IBD is unknown, but clear evidence suggests that intestinal inflammation is caused by an excessive immune response to mucosal antigens. Recent studies have shown that activation of the aryl hydrocarbon receptor (AhR) induces regulatory T cells (Tregs) and suppresses autoimmune diseases. In the current study, we investigated if a nontoxic ligand of AhR, 2-(1′ H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE), can attenuate dextran sodium sulfate-induced colitis. Our studies demonstrated that in mice that received ITE treatment in vivo, colitis pathogenesis, including a decrease in body weight, was significantly reversed along with the systemic and intestinal inflammatory cytokines. ITE increased the expression of Tregs in spleen, mesenteric lymph nodes (MLNs), and colon lamina propria lymphocytes (cLPL) of mice with colitis when compared with controls. This induction of Tregs was reversed by AhR antagonist treatment in vitro. ITE treatment also increased dendritic cells (CD11c+) and decreased macrophages (F4/80+) from the spleen, MLNs, and cLPL in mice with colitis. ITE also reversed the systemic and intestinal frequency of CD4+T cells during colitis and suppressed inflammatory cytokines including IFN-γ, TNF-α, IL-17, IL-6, and IL-1 as well as induced IL-10 levels. These findings suggest that ITE attenuates colitis through induction of Tregs and reduction in inflammatory CD4+T cells and cytokines. Therefore, our work demonstrates that the nontoxic endogenous AhR ligand ITE may serve as a therapeutic modality to treat IBD.NEW & NOTEWORTHY We report the novel finding that activation of the aryl hydrocarbon receptor with the nontoxic ligand 2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) induces regulatory T cells (Tregs) and suppresses inflammatory bowel disease (IBD). Our data suggest that ITE diminishes colitis pathology through induction of Tregs; reduces inflammatory cytokines, inflammation score, and macrophage frequency; and induces DCs resulting in amelioration of colitis. Therefore, nontoxic endogenous ITE promotes the induction of Tregs and may be useful for the treatment of IBD.

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