ArticleNature immunology2011
AHR drives the development of gut ILC22 cells and postnatal lymphoid tissues via pathways dependent on and independent of Notch.
Article in Nature immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 468 papers, 1 of them a synthesis that pooled it.
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Who cites it
468 citing papers in PubMed, 1 synthesis or guideline pooled it, 758 citations in OpenAlex.
- Influence of Alcohol on the Intestinal Immune System.Alcohol research : current reviews · 2025Pooled it
- Inhibition of Aryl hydrocarbon receptor Interleukin-22 signaling and worsening of intestinal inflammation byGut microbes · 2026Article
- ILC3s as central regulators of mucosal homeostasis and disease pathogenesis (Review).International journal of molecular medicine · 2026Review
- Plasticity of the infant immune system during the perinatal period.Nature reviews. Immunology · 2026Review
- Climate Change-Mediated Temperature Extremes: Effects on the Immune System and Associations with Immune-Related Diseases.Clinical reviews in allergy & immunology · 2026Review
- AHR-Responsive Carbon Dots Orchestrate Skin Wound Healing and Colonic Mucosal Repair via Treg-Mediated Macrophage Efferocytosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Role of the Gut Microbiota in Allogeneic Hematopoietic Cell Transplantation.American journal of hematology · 2026Review
- Crohn's Disease: From Immune Dysregulation to Intestinal Damage.Inflammation · 2026Review
- AhR as a Common Denominator in Immunity and Inflammation in Chronic Lung Diseases: Molecular and Clinical Insights.Diseases (Basel, Switzerland) · 2026Review
- LINGO4 coordinates ILC3-intrinsic IL-22 production and microbiota-mediated ILC3 homeostasis.The Journal of experimental medicine · 2026Article
- Tfam-mediated metabolic perturbation in RORγtCell reports · 2026Article
- Early-Life Gut Microbiota: Education of the Immune System and Links to Autoimmune Diseases.Microorganisms · 2026Review
- Microbiota-derived metabolites in hematopoietic regulation and disease: mechanisms, context, and therapeutic perspectives.Frontiers in microbiology · 2026Review
- Evaluation of Indigo Naturalis Prepared Using a Novel Method: Anti-Inflammatory Activities Against Colonic Cancer Cell Lines.Mediators of inflammation · 2026Article
- Modified Jiaoqi powder ameliorates ulcerative colitis through gut microbiota-tryptophan metabolism-AhR signaling modulating-ILC2/ILC3 balance.Frontiers in microbiology · 2026Article
- Inflammatory bowel disease through the lens of microbe-host interactions: immunomodulation, metabolic effects, and genetic susceptibility in microbiota dysbiosis.Frontiers in cellular and infection microbiology · 2026Review
- Tryptophan Indole Metabolites Reduce Anastomotic Leakage Through Aryl Hydrocarbon Receptor-Driven Interleukin-22 Production.Cellular and molecular gastroenterology and hepatology · 2026Article
- High-dose capsaicin exposure is associated with more severe inflammation, intestinal dysregulation, and IL-17 elevation in experimental autoimmune uveitis.Frontiers in microbiology · 2026Article
- A "One-Stone-Three-Birds" Inspired Nanoplatform for Multitargeted Ulcerative Colitis Therapy via Combined Aryl Hydrocarbon Receptor Activation and Reactive Oxygen Species Scavenging.Biomaterials research · 2026Article
- Physiological activation of Aryl hydrocarbon receptor by food-derived ligands is essential for the efficacy of anti-PD1 therapy.Nature communications · 2025Article
408 more citing papers are in PubMed but not listed here.
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11 authors at 2 institutions in 1 country.
Funding
Abstract
Innate lymphoid cells (ILCs) of the ILC22 type protect the intestinal mucosa from infection by secreting interleukin 22 (IL-22). ILC22 cells include NKp46(+) and lymphoid tissue-inducer (LTi)-like subsets that express the aryl hydrocarbon receptor (AHR). Here we found that Ahr(-/-) mice had a considerable deficit in ILC22 cells that resulted in less secretion of IL-22 and inadequate protection against intestinal bacterial infection. Ahr(-/-) mice also lacked postnatally 'imprinted' cryptopatches and isolated lymphoid follicles (ILFs), but not embryonically 'imprinted' Peyer's patches. AHR induced the transcription factor Notch, which was required for NKp46(+) ILCs, whereas LTi-like ILCs, cryptopatches and ILFs were partially dependent on Notch signaling. Thus, AHR was essential for ILC22 cells and postnatal intestinal lymphoid tissues. Moreover, ILC22 subsets were heterogeneous in their requirement for Notch and their effect on the generation of intestinal lymphoid tissues.
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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.