ArticleImmunity2012
Th22 cells are an important source of IL-22 for host protection against enteropathogenic bacteria.
Article in Immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 287 papers.
What it found
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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.
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Who cites it
287 citing papers in PubMed, 444 citations in OpenAlex.
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- Aryl hydrocarbon receptor pharmacology-mechanisms, ligands, and therapeutic potential.Pharmacological reviews · 2026Review
- Why, Immunologically, Housing-Related Fungi and Endotoxins (and Other Chronic Pro-Inflammatory Stressors) Risk Latent Tuberculosis Reactivation, Severe Asthma, and Translocating and Invasive Infections in Indigenous Communities in Canada.American journal of human biology : the official journal of the Human Biology Council · 2026Review
- Cell type-specific enhancers regulate IL-22 expression in innate and adaptive type 3 lymphoid cells.Nature communications · 2026Article
- Assessment of Serum Interleukins 18 and 22 in Predicting Neonatal Sepsis and Mortality: A Case-Control Study.Clinical medicine insights. Pediatrics · 2026Article
- Kinetics of Biomarkers for Therapeutic Assessment in Swiss Mice Infected with a VirulentPathogens (Basel, Switzerland) · 2026Article
- The aryl hydrocarbon receptor: structure, signaling, physiology and pathology.Signal transduction and targeted therapy · 2026Review
- Gut Microbiota and Interorgan Communication Among the Gut, Brain, and Beyond.Internal medicine (Tokyo, Japan) · 2026Review
- Aryl Hydrocarbon Receptor Ligands Drive Pancreatic Cancer Initiation and Progression through Protumorigenic T-cell Polarization.Cancer discovery · 2026Article
- Therapeutic potential of ginseng and its bioactive compounds in inflammatory bowel disease: current evidence and future directions.Frontiers in immunology · 2026Review
- MAIT Cells Maintain Intestinal Homeostasis Through IL-22 in an Experimental Colitis.Journal of inflammation research · 2026Article
- Rehydration rescues Il22Nature communications · 2025Article
- Beneficial and detrimental consequences of AHR activation in intestinal infection.Life science alliance · 2025Article
- The accessory type III secretion system effectors collectively shape intestinal inflammatory infection outcomes.Gut microbes · 2025Article
- In vitro models to mimic tumor endothelial cell-mediated immune cell reprogramming in lung adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2025Article
- Phantom of the immunologic opera: Unmasking the role of innate lymphoid cells (ILC) in inborn errors of immunity (IEI).Journal of human immunity · 2025Review
- Endothelial cell-ILC3 crosstalk via the ET-1/EDNRA axis promotes NKp46Cellular & molecular immunology · 2025Article
- T cell cholesterol transport links intestinal immune responses to dietary lipid absorption.Science (New York, N.Y.) · 2025Article
227 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Interleukin-22 (IL-22) is central to host protection against bacterial infections at barrier sites. Both innate lymphoid cells (ILCs) and T cells produce IL-22. However, the specific contributions of CD4(+) T cells and their developmental origins are unclear. We found that the enteric pathogen Citrobacter rodentium induced sequential waves of IL-22-producing ILCs and CD4(+) T cells that were each critical to host defense during a primary infection. Whereas IL-22 production by ILCs was strictly IL-23 dependent, development of IL-22-producing CD4(+) T cells occurred via an IL-6-dependent mechanism that was augmented by, but not dependent on, IL-23 and was dependent on both transcription factors T-bet and AhR. Transfer of CD4(+) T cells differentiated with IL-6 in the absence of TGF-β ("Th22" cells) conferred complete protection of infected IL-22-deficient mice whereas transferred Th17 cells did not. These findings establish Th22 cells as an important component of mucosal antimicrobial host defense.
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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.