ArticleThe Journal of experimental medicine2022
The aryl hydrocarbon receptor contributes to tissue adaptation of intestinal eosinophils in mice.
Article in The Journal of experimental medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 65 citations in OpenAlex.
- Review
- Rediscovering eosinophil identity through tissue adaptation.Nature immunology · 2026Review
- Eosinophils promote a second wave of postnatal smooth muscle differentiation in intestinal villi.The Journal of cell biology · 2026Article
- Tissue adaptation of eosinophils.Journal of leukocyte biology · 2026Review
- Article
- Review
- [Research Progress on the Biological Functions of Intestinal Eosinophils and Related Diseases].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026Review
- Mapping the spatiotemporal adaptation of eosinophils.Nature immunology · 2026Article
- The aryl hydrocarbon receptor is expressed in non-sensory cells in the cochlea and regulates hair cell survival.Frontiers in molecular neuroscience · 2026Article
- Tryptophan Indole Metabolites Reduce Anastomotic Leakage Through Aryl Hydrocarbon Receptor-Driven Interleukin-22 Production.Cellular and molecular gastroenterology and hepatology · 2026Article
- Physiological activation of Aryl hydrocarbon receptor by food-derived ligands is essential for the efficacy of anti-PD1 therapy.Nature communications · 2025Article
- Beneficial and detrimental consequences of AHR activation in intestinal infection.Life science alliance · 2025Article
- GPR43 in eosinophils suppresses the emergence of pathogenic Siglec-FNature communications · 2025Article
- Epigenetic and transcriptional programming of murine eosinophils in the esophagus.Nature communications · 2025Article
- Review
- Unsupervised Clustering Reveals Intestine-Adapted Eosinophil Subsets Shaped by Local Inflammation.Allergy · 2025Article
- Aryl Hydrocarbon Receptor Activation Promotes Effector CD4+ T Cell Homeostasis and Restrains Salt-Sensitive Hypertension.Function (Oxford, England) · 2025Article
- The role of the AHR in host-pathogen interactions.Nature reviews. Immunology · 2025Review
- Single-cell RNA sequencing of human blood eosinophils reveals plasticity and absence of canonical cell subsets.Allergy · 2025Article
- The Role of Fibroblasts in Atopic Dermatitis: Establishing Proinflammatory Microenvironments and Mediating Cellular Crosstalk.Journal of inflammation research · 2025Review
Corrections and comments
- Commented on by
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Eosinophils are potent sources of inflammatory and toxic mediators, yet they reside in large numbers in the healthy intestine without causing tissue damage. We show here that intestinal eosinophils were specifically adapted to their environment and underwent substantial transcriptomic changes. Intestinal eosinophils upregulated genes relating to the immune response, cell-cell communication, extracellular matrix remodeling, and the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor with broad functions in intestinal homeostasis. Eosinophils from AHR-deficient mice failed to fully express the intestinal gene expression program, including extracellular matrix organization and cell junction pathways. AHR-deficient eosinophils were functionally impaired in the adhesion to and degradation of extracellular matrix, were more prone to degranulation, and had an extended life span. Lack of AHR in eosinophils had wider effects on the intestinal immune system, affecting the T cell compartment in nave and helminth-infected mice. Our study demonstrates that the response to environmental triggers via AHR partially shapes tissue adaptation of eosinophils in the small intestine.
Indexed as
Identifiers
What OpenQuestion holds
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.