ArticleNature immunology2016
Interferon and IL-27 antagonize the function of group 2 innate lymphoid cells and type 2 innate immune responses.
Article in Nature immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 254 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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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
254 citing papers in PubMed, 381 citations in OpenAlex.
- Pulmonary Innate Lymphoid Cell Responses during Rhinovirus-induced Asthma ExacerbationsAmerican journal of respiratory and critical care medicine · 2021Trial
- Impacts of Environmental Pollutants on Innate Immunity: The Role of Group 2 Innate Lymphoid Cells.Clinical reviews in allergy & immunology · 2026Review
- Humanizing acidic mammalian chitinase variants establish lung immune conditioning and control environmentally driven inflammation and fibrosis.Cell reports · 2026Article
- Cytokine multimerization: when more is more and sometimes less.Nature reviews. Immunology · 2026Review
- An early protective effect of IL-9 in murine systemic lupus erythematosus.ImmunoHorizons · 2026Article
- Spatial and Phenotypic Heterogeneity of ILC Subsets in Mouse Lung Under Type 2 Inflammatory Conditions.European journal of immunology · 2026Article
- Androgens protect ILC2S from functional suppression during influenza virus infection.Mucosal immunology · 2026Article
- Metabolic Reprogramming and ILC2 Plasticity in Obesity-related Asthma.Clinical reviews in allergy & immunology · 2026Review
- Gut-derived, inflammatory ILC2s disseminate type 2 immunity to remote lung in food allergen-challenged mice.Journal of leukocyte biology · 2026Article
- STAT4 drives optimal expansion and transcriptional repression of type I interferon pathway in inflammatory ILC2.Cellular and molecular life sciences : CMLS · 2026Article
- Distinguishing Features of ILC2s During Type 2 Immune Responses.European journal of immunology · 2026Review
- Early life group 2 innate lymphoid cells in health and disease.Molecular and cellular pediatrics · 2026Review
- IFN-γ-dominant immune shift is associated with reduced protective ILC2 responses in chronic kidney disease.Frontiers in immunology · 2026Article
- The gut-lung axis: pathological crosstalk and inter-organ communication in chronic obstructive pulmonary disease and inflammatory bowel disease.Frontiers in immunology · 2026Review
- The IL-33-ILC2 axis: a key regulator of type 2 immunity in respiratory disease.Frontiers in immunology · 2026Review
- Clostridium scindens attenuates acute kidney injury by producing indole-3-acetic acid.NPJ biofilms and microbiomes · 2025Article
- Ligand-receptor interactions induce and mediate regulatory functions of BATF3Science advances · 2025Article
- ICOS regulates IL-10 production in group 2 innate lymphoid cells via cholesterol and cortisol biosynthesis.The Journal of clinical investigation · 2025Article
- Unraveling the mechanisms of virus-induced asthma exacerbation: epithelial injury, immune dysregulation, and novel interventions.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Innate Lymphoid Cells Are the Rheostat of Immune Response in the Kidney.Journal of cellular and molecular medicine · 2025Review
194 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
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group 2 innate lymphoid cells (ILC2 cells) are type 2 cytokine-producing cells of the innate immune system with important roles in helminth infection and allergic inflammation. Here we found that tissue-resident ILC2 cells proliferated in situ without migrating during inflammatory responses. Both type I and type II interferons and interleukin 27 (IL-27) suppressed ILC2 function in a manner dependent on the transcription factor STAT1. ILC2-mediated lung inflammation was enhanced in the absence of the interferon-γ (IFN-γ) receptor on ILC2 cells in vivo. IFN-γ effectively suppressed the function of tissue-resident ILC2 cells but not that of inflammatory ILC2 cells, and IL-27 suppressed tissue-resident ILC2 cells but not tissue-resident TH2 cells during lung inflammation induced by Alternaria alternata. Our results demonstrate that suppression mediated by interferon and IL-27 is a negative feedback mechanism for ILC2 function in vivo.
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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.