ArticleToxicological sciences : an official journal of the Society of Toxicology2018
TCDD, FICZ, and Other High Affinity AhR Ligands Dose-Dependently Determine the Fate of CD4+ T Cell Differentiation.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 132 citations in OpenAlex.
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- AHR-Responsive Carbon Dots Orchestrate Skin Wound Healing and Colonic Mucosal Repair via Treg-Mediated Macrophage Efferocytosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- In vitro characterization of the role of aryl hydrocarbon receptor and bisphenol A on IL-17A regulation in mouse and human CD4+ T cells.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- [Role of AHR-mediated histone acetylation at FOXP3 in Tfr cell differentiation in systemic lupus erythematosus].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Article
- Aryl hydrocarbon receptor deficiency triggers the activation of γδT17 cells to exacerbate autoimmune inflammation.Science advances · 2026Article
- CYP1A1 as a conserved metabolic circuit linking environmental sensing to immune regulation.Archives of toxicology · 2026Review
- Aryl Hydrocarbon Receptor Signaling in Aging: A Key Modulator of Brain Homeostasis.Molecular neurobiology · 2026Review
- AHR: The Overlooked Mediator in SkincareBridging Environmental Sensing and Skin Physiology.Environment & health (Washington, D.C.) · 2026Review
- Metabolic reprogramming of Th17/Treg imbalance in autoimmune thyroid diseases.Cell communication and signaling : CCS · 2026Review
- Plant extract mixture shows anti-inflammatory and barrier-strengthening effects and activates aryl hydrocarbon receptor in a 2D psoriasis model.Scientific reports · 2026Article
- Review
- Aryl hydrocarbon receptor activation alters emergency hematopoiesis during influenza A virus infection.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- The aryl hydrocarbon receptor: structure, signaling, physiology and pathology.Signal transduction and targeted therapy · 2026Review
- Ultraviolet radiation as a double-edged regulator of melanocyte function in vitiligo therapy and melanoma carcinogenesis.Frontiers in medicine · 2026Review
- Aryl hydrocarbon receptor: a multifaceted environmental sensor in liver homeostasis and disease.Frontiers in medicine · 2026Review
- An Ecofriendly L-Tryptophan Containing UVA-1 Permissive Sunscreen Formulation: A Novel Approach for Inflammatory and Fibrosing Skin Diseases.International journal of tryptophan research : IJTR · 2026Article
- Metabolic checkpoints in the regulation of Th17 cells: implications for uveitis pathogenesis and therapy.Frontiers in immunology · 2026Review
- Targeting the gut-lung axis in COPD: from microbial metabolites to fecal microbiota transplantation.Frontiers in microbiology · 2026Review
- Reprogramming offspring liver health: maternal indole supplementation as a preventive strategy against MASLD.EBioMedicine · 2026Article
- Article
39 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
FICZ and TCDD, two high-affinity AhR ligands, are reported to have opposite effects on T cell differentiation with TCDD inducing regulatory T cells and FICZ inducing Th17 cells. This dichotomy has been attributed to ligand-intrinsic differences in AhR activation, although differences in sensitivity to metabolism complicate the issue. TCDD is resistant to AhR-induced metabolism and produces sustained AhR activation following a single dose in the μg/kg range, whereas FICZ is rapidly metabolized and AhR activation is transient. Nonetheless, prior studies comparing FICZ with TCDD have generally used the same 10-50 μg/kg dose range, and thus the two ligands would not equivalently activate AhR. We hypothesized that high-affinity AhR ligands can promote CD4+ T cell differentiation into both Th17 cells and Tregs, with fate depending on the extent and duration of AhR activation. We compared the immunosuppressive effects of TCDD and FICZ, along with two other rapidly metabolized ligands (ITE and 11-Cl-BBQ) in an acute alloresponse mouse model. The dose and timing of administration of each ligand was optimized for TCDD-equivalent Cyp1a1 induction. When optimized, all of the ligands suppressed the alloresponse in conjunction with the induction of Foxp3- Tr1 cells on day 2 and the expansion of natural Foxp3+ Tregs on day 10. In contrast, a low dose of FICZ induced transient expression of Cyp1a1 and did not induce Tregs or suppress the alloresponse but enhanced IL-17 production. Interestingly, low doses of the other ligands, including TCDD, also increased IL-17 production on day 10. These findings support the conclusion that the dose and the duration of AhR activation by high-affinity AhR ligands are the primary factors driving the fate of T cell differentiation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.