ArticlePloS one2015
The Group 3 Innate Lymphoid Cell Defect in Aryl Hydrocarbon Receptor Deficient Mice Is Associated with T Cell Hyperactivation during Intestinal Infection.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
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.
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Who cites it
28 citing papers in PubMed, 38 citations in OpenAlex.
- Article
- The thin line between conventional dendritic cells (cDCs) and group 3 innate lymphoid cells (ILC3s) in the gut.International immunology · 2023Article
- ILCs-Crucial Players in Enteric Infectious Diseases.International journal of molecular sciences · 2022Review
- Impact of MyD88, Microbiota, and Location on Type 1 and Type 3 Innate Lymphoid Cells duringImmunoHorizons · 2022Article
- Microbial Tryptophan Metabolism Tunes Host Immunity, Metabolism, and Extraintestinal Disorders.Metabolites · 2022Review
- Transcription factor-driven regulation of ILC1 and ILC3.Trends in immunology · 2022Review
- Intestinal immune responses to commensal and pathogenic protozoa.Frontiers in immunology · 2022Review
- Nuclear receptors: a bridge linking the gut microbiome and the host.Molecular medicine (Cambridge, Mass.) · 2021Review
- Induction of IL-12p40 and type 1 immunity by Toxoplasma gondii in the absence of the TLR-MyD88 signaling cascade.PLoS pathogens · 2021Article
- Rodent genetic models of Ah receptor signaling.Drug metabolism reviews · 2021Review
- Indole-3-Carbinol-Dependent Aryl Hydrocarbon Receptor Signaling Attenuates the Inflammatory Response in Experimental Necrotizing Enterocolitis.ImmunoHorizons · 2021Article
- ILC3, a Central Innate Immune Component of the Gut-Brain Axis in Multiple Sclerosis.Frontiers in immunology · 2021Review
- The role of innate lymphoid cells in response to microbes at mucosal surfaces.Mucosal immunology · 2020Review
- Interleukin-17 mediated immunity during infections with Trypanosoma cruzi and other protozoans.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- From Initiators to Effectors: Roadmap Through the Intestine During Encounter ofFrontiers in cellular and infection microbiology · 2020Review
- Innate, adaptive, and cell-autonomous immunity against Toxoplasma gondii infection.Experimental & molecular medicine · 2019Review
- The aryl hydrocarbon receptor: an environmental sensor integrating immune responses in health and disease.Nature reviews. Immunology · 2019Review
- Group 3 ILCs: Peacekeepers or Troublemakers? What's Your Gut Telling You?!Frontiers in immunology · 2019Review
- Innate Lymphoid Cells in Protection, Pathology, and Adaptive Immunity During Apicomplexan Infection.Frontiers in immunology · 2019Review
- AHR signaling in the development and function of intestinal immune cells and beyond.Seminars in immunopathology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Intestinal infection with the intracellular parasite Toxoplasma gondii results in the translocation of commensal bacteria to peripheral organs and the development of a T cell response specific to the microbiota. In naïve mice, the recently described RORγt+ group 3 innate lymphoid cell (ILC) population plays a critical role in promoting intestinal barrier function and limiting responses to gut-resident commensal bacteria. Given this role for group 3 ILCs, studies were performed to evaluate whether these cells might influence the immune response to mucosal infection with T. gondii. Phenotypic characterization of RORγt+ ILCs in T. gondii infected mice revealed that this population decreased following challenge but the population that remained expressed costimulatory molecules and IL-22. One factor that influences the maintenance of RORγt+ ILCs is the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor, and Ahr-/- mice have a marked defect in the lamina propria group 3 ILC population. When Ahr-/- mice were challenged with T. gondii, they lost more weight than wild type controls. This disease course in Ahr-/- animals was associated with increased T cell responses to Toxoplasma antigen and crude commensal antigen preparations. Together, these data suggest that group 3 ILCs have a role in limiting T cell activation during intestinal infection.
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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.