ArticleNature immunology2016
Inflammatory triggers associated with exacerbations of COPD orchestrate plasticity of group 2 innate lymphoid cells in the lungs.
Article in Nature immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 279 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
279 citing papers in PubMed.
- INEXAS: A Phase 2 Randomized Trial of On-demand Inhaled Interferon Beta-1a in Severe Asthmatics.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2021Trial
- Innate Lymphoid Cells Activation and Transcriptomic Changes in Response to Human Dengue Infection.Frontiers in immunology · 2021Trial
- Respiratory mucosal immunity: Biological functions, diseases, prevention and therapy.Genes & diseases · 2026Review
- Type I IFN promotes ILC2-to-ILC1 plasticity in pre-clinical radiation-induced lung injury.Nature communications · 2026Article
- Peripheral blood innate lymphoid cell profiles of patients with COPD reflect their clinical phenotype as identified by cluster analysis.BMJ open respiratory research · 2026Article
- Impacts of Environmental Pollutants on Innate Immunity: The Role of Group 2 Innate Lymphoid Cells.Clinical reviews in allergy & immunology · 2026Review
- Integrative Omics of Eosinophils in Asthma and COPD: Deciphering Molecular Signatures for Targeted Therapy.Molecular diagnosis & therapy · 2026Review
- Influenza-induced tuft cell expansion is associated with changes in ILC2 populations in the distal lungs of mice.Physiological reports · 2026Article
- Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026Review
- Mast cells and endothelial cells mediate interleukin-33 and ST2 responses in distal chronic obstructive pulmonary disease lungs.American journal of respiratory and critical care medicine · 2026Article
- IL-9 and Blimp-1 protect the transcriptional identity of group 2 innate lymphocytes in allergic asthma.Nature immunology · 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
- Review
- Review
- Microbiota-driven mechanisms in multisystem diseases: integrative evidence across cardiovascular, metabolic, neurological and autoimmune disorders.Antonie van Leeuwenhoek · 2026Review
- STAT4 drives optimal expansion and transcriptional repression of type I interferon pathway in inflammatory ILC2.Cellular and molecular life sciences : CMLS · 2026Article
- The context-dependent role of group 2 innate lymphoid cells in lung diseases.Acta biochimica et biophysica Sinica · 2026Review
- The IL-33-ILC2 axis: a key regulator of type 2 immunity in respiratory disease.Frontiers in immunology · 2026Review
219 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
13 authors.
Funding
Abstract
Innate lymphoid cells (ILCs) are critical mediators of mucosal immunity, and group 1 ILCs (ILC1 cells) and group 3 ILCs (ILC3 cells) have been shown to be functionally plastic. Here we found that group 2 ILCs (ILC2 cells) also exhibited phenotypic plasticity in response to infectious or noxious agents, characterized by substantially lower expression of the transcription factor GATA-3 and a concomitant switch to being ILC1 cells that produced interferon-γ (IFN-γ). Interleukin 12 (IL-12) and IL-18 regulated this conversion, and during viral infection, ILC2 cells clustered within inflamed areas and acquired an ILC1-like phenotype. Mechanistically, these ILC1 cells augmented virus-induced inflammation in a manner dependent on the transcription factor T-bet. Notably, IL-12 converted human ILC2 cells into ILC1 cells, and the frequency of ILC1 cells in patients with chronic obstructive pulmonary disease (COPD) correlated with disease severity and susceptibility to exacerbations. Thus, functional plasticity of ILC2 cells exacerbates anti-viral immunity, which may have adverse consequences in respiratory diseases such as COPD.
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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.