ReviewFrontiers in immunology2017
Group 3 Innate Lymphoid Cells: Communications Hubs of the Intestinal Immune System.
Review in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed, 94 citations in OpenAlex.
- Understanding the Variability of Peanut-Oral Immunotherapy Responses by Multi-Omics Profiling of Immune Cells.Allergy · 2025Trial
- 12R-HETE acts as an endogenous ligand for Nur77 in the intestines and regulates NKp46Science advances · 2026Article
- Alterations in mucosa branchedGut microbes · 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
- The interaction network between group 3 innate lymphoid cells and other cells.Fundamental research · 2025Review
- The Interplay between the Gut and Ketogenic Diets in Health and Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Circulating subpopulations of non-cytotoxic ILCs in diffuse large B-cell lymphoma.Annals of hematology · 2025Article
- Group 3 Innate Lymphoid Cells: A Potential Therapeutic Target for Steroid Resistant Asthma.Clinical reviews in allergy & immunology · 2024Review
- The Role of Retinoic-Acid-Related Orphan Receptor (RORs) in Cellular Homeostasis.International journal of molecular sciences · 2024Review
- Efficient enzyme-free method to assess the development and maturation of the innate and adaptive immune systems in the mouse colon.Scientific reports · 2024Article
- Serotonin Transporter Deficiency Induces Metabolic Alterations in the Ileal Mucosa.International journal of molecular sciences · 2024Article
- Dysregulation of Wnt/β-catenin signaling contributes to intestinal inflammation through regulation of group 3 innate lymphoid cells.Nature communications · 2024Article
- Blockade of C5aR1 resets M1 via gut microbiota-mediated PFKM stabilization in a TLR5-dependent manner.Cell death & disease · 2024Article
- Investigating the Influence of Gut Microbiota-related Metabolites in Gastrointestinal Cancer.Current cancer drug targets · 2024Review
- Disease pathogenesis and barrier functions regulated by group 3 innate lymphoid cells.Seminars in immunopathology · 2024Review
- Divergent roles for STAT4 in shaping differentiation of cytotoxic ILC1 and NK cells during gut inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- The thin line between conventional dendritic cells (cDCs) and group 3 innate lymphoid cells (ILC3s) in the gut.International immunology · 2023Article
- Circular RNAs in inflammatory bowel disease.Frontiers in immunology · 2023Review
- Ornithine decarboxylase supports ILC3 responses in infectious and autoimmune colitis through positive regulation of IL-22 transcription.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The maintenance of mammalian health requires the generation of appropriate immune responses against a broad range of environmental and microbial challenges, which are continually encountered at barrier tissue sites including the skin, lung, and gastrointestinal tract. Dysregulated barrier immune responses result in inflammation, both locally and systemically in peripheral organs. Group 3 innate lymphoid cells (ILC3) are constitutively present at barrier sites and appear to be highly specialized in their ability to sense a range of environmental and host-derived signals. Under homeostatic conditions, ILC3 respond to local cues to maintain tissue homeostasis and restrict inflammatory responses. In contrast, perturbations in the tissue microenvironment resulting from disease, infection, or tissue damage can drive dysregulated pro-inflammatory ILC3 responses and contribute to immunopathology. The tone of the ILC3 response is dictated by a balance of "exogenous" signals, such as dietary metabolites and commensal microbes, and "endogenous" host-derived signals from stromal cells, immune cells, and the nervous system. ILC3 must therefore have the capacity to simultaneously integrate a wide array of complex and dynamic inputs in order to regulate barrier function and tissue health. In this review, we discuss the concept of ILC3 as a "communications hub" in the intestinal tract and associated lymphoid tissues and address the variety of signals, derived from multiple biological systems, which are interpreted by ILC3 to modulate the release of downstream effector molecules and regulate cell-cell crosstalk. Successful integration of environmental cues by ILC3 and downstream propagation to the broader immune system is required to maintain a tolerogenic and anti-inflammatory tone and reinforce barrier function, whereas dysregulation of ILC3 responses can contribute to the onset or progression of clinically relevant chronic inflammatory diseases.
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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.