ArticleeLife2023
Homeostatic activation of aryl hydrocarbon receptor by dietary ligands dampens cutaneous allergic responses by controlling Langerhans cells migration.
Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- The aryl hydrocarbon receptor: structure, signaling, physiology and pathology.Signal transduction and targeted therapy · 2026Review
- Physiological activation of Aryl hydrocarbon receptor by food-derived ligands is essential for the efficacy of anti-PD1 therapy.Nature communications · 2025Article
- Aryl hydrocarbon receptor restrains tonic cytokine responses by inhibiting microbiota sensing in monocytes.The Journal of clinical investigation · 2025Article
- The aryl hydrocarbon receptor: a rehabilitated target for therapeutic immune modulation.Nature reviews. Drug discovery · 2025Review
- Dietary lipids are largely deposited in skin and rapidly affect insulating properties.Nature communications · 2025Article
- Striking a balance: new perspectives on homeostatic dendritic cell maturation.Nature reviews. Immunology · 2025Review
- Convergent evolution of monocyte differentiation in adult skin instructs Langerhans cell identity.Science immunology · 2024Article
- Mechanisms underlying aryl hydrocarbon receptor-driven divergent macrophage function.Toxicological sciences : an official journal of the Society of Toxicology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dietary compounds can affect the development of inflammatory responses at distant sites. However, the mechanisms involved remain incompletely understood. Here, we addressed the influence on allergic responses of dietary agonists of aryl hydrocarbon receptor (AhR). In cutaneous papain-induced allergy, we found that lack of dietary AhR ligands exacerbates allergic responses. This phenomenon was tissue-specific as airway allergy was unaffected by the diet. In addition, lack of dietary AhR ligands worsened asthma-like allergy in a model of 'atopic march.' Mice deprived of dietary AhR ligands displayed impaired Langerhans cell migration, leading to exaggerated T cell responses. Mechanistically, dietary AhR ligands regulated the inflammatory profile of epidermal cells, without affecting barrier function. In particular, we evidenced TGF-β hyperproduction in the skin of mice deprived of dietary AhR ligands, explaining Langerhans cell retention. Our work identifies an essential role for homeostatic activation of AhR by dietary ligands in the dampening of cutaneous allergic responses and uncovers the importance of the gut-skin axis in the development of allergic diseases.
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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.