ArticleImmunoHorizons2019
IL-21 Controls ILC3 Cytokine Production and Promotes a Protective Phenotype in a Mouse Model of Colitis.
Article in ImmunoHorizons, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 15 citations in OpenAlex.
- Establishing the PMThe Journal of allergy and clinical immunology · 2026Article
- Roles of glucagon-like peptide 1 receptor agonists in immune cell biology and autoimmune/autoinflammatory diseases.Cell & bioscience · 2025Review
- Tertiary lymphoid structures in diseases: immune mechanisms and therapeutic advances.Signal transduction and targeted therapy · 2024Review
- Single-cell sequencing reveals the evolution of immune molecules across multiple vertebrate species.Journal of advanced research · 2024Article
- The Biological Functions and Intestinal Inflammation Regulation of IL-21 in Grass Carp (Cells · 2023Article
- Microbiota as key factors in inflammatory bowel disease.Frontiers in microbiology · 2023Review
- ILC3: a case of conflicted identity.Frontiers in immunology · 2023Review
- Impact of MyD88, Microbiota, and Location on Type 1 and Type 3 Innate Lymphoid Cells duringImmunoHorizons · 2022Article
- Inflammatory Bowel Disease: A Review of Pre-Clinical Murine Models of Human Disease.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Group 3 innate lymphoid cells (ILC3s) have dual roles in intestinal health, acting in both protective and pathogenic capacities, and importantly, modulations in this population of innate lymphoid cells have been implicated in inflammatory bowel disease. Further, subpopulations of ILC3s have been described as serving specific functions in maintaining homeostasis or responding to infection, and aberrant activation of one or more of these subpopulations could exacerbate inflammatory bowel disease. However, the signals that enforce the protective and pathogenic features of ILC3s are not fully elucidated. In this article, we show that IL-21, a cytokine primarily produced by CD4 T cells, acts on a subpopulation of intestinal ILC3s to promote a protective phenotype. IL-21 signaling does not affect the MHC class II-expressing ILC3 subset but promotes ILC3s that express Tbet and are poised to produce IL-22. Consistent with a protective phenotype, IL-21 deficiency dampens cytokine-induced IL-17A production. We show that exacerbated colitis develops in mice lacking the IL-21 receptor, in agreement with a protective role for IL-21 signaling on ILC3s. To our knowledge, these data reveal a novel role for IL-21 in shaping innate lymphoid cell responses in the intestine and provide one mechanism by which effector CD4 T cells can influence innate immunity.
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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.