ArticleMucosal immunology2018
IFN-γ increases susceptibility to influenza A infection through suppression of group II innate lymphoid cells.
Article in Mucosal immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.
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
105 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.
- SARS-CoV-2 Causes a Different Cytokine Response Compared to Other Cytokine Storm-Causing Respiratory Viruses in Severely Ill Patients.Frontiers in immunology · 2021Pooled it
- Androgens protect ILC2S from functional suppression during influenza virus infection.Mucosal immunology · 2026Article
- Spatial and Phenotypic Heterogeneity of ILC Subsets in Mouse Lung Under Type 2 Inflammatory Conditions.European journal of immunology · 2026Article
- Lung adventitial fibroblasts support type 2 Tregs to shape the response to influenza infection.bioRxiv : the preprint server for biology · 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
- Myeloid cell expression of the VDR and parathyroid hormone control the host response to influenza infection in mice.Frontiers in immunology · 2026Article
- T-cell immunity against influenza virus does not require Th1 or Th17 master regulator transcription factors.Mucosal immunology · 2025Article
- Obesity Risk Factors Promote Metabolic Reprogramming and Viral Infection in Airways with Type 1 High Inflammation.Biomolecules · 2025Article
- ILC2 Diversity, Location, and Function in Pulmonary Disease.Immunological reviews · 2025Review
- Baicalin restores innate lymphoid immune imbalance during exacerbation of COPD.Immunologic research · 2025Article
- Putting computational models of immunity to the test-An invited challenge to predict B.pertussis vaccination responses.PLoS computational biology · 2025Article
- Tissue-resident immune cells: from defining characteristics to roles in diseases.Signal transduction and targeted therapy · 2025Review
- Effects and Mechanisms of Silibinin on Influenza A/H1N1 Pathogenesis in a Mouse Model.Journal of tropical medicine · 2025Article
- Can invariant Natural Killer T cells drive B cell fate? a look at the humoral response.Frontiers in immunology · 2025Review
- Lung-resident lymphocytes and their roles in respiratory infections and chronic respiratory diseases.Chinese medical journal pulmonary and critical care medicine · 2024Review
- Treatment with lipoxin AInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- An ILC2-chitinase circuit restores lung homeostasis after epithelial injury.Science immunology · 2024Article
- Viral infection induces inflammatory signals that coordinate YAP regulation of dysplastic cells in lung alveoli.The Journal of clinical investigation · 2024Article
- Tissue-specific features of innate lymphoid cells in antiviral defense.Cellular & molecular immunology · 2024Review
45 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
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Increased levels of interferon-γ (IFN-γ) are routinely observed in the respiratory tract following influenza virus infection, yet its potential role remains unclear. We now demonstrate that influenza-induced IFN-γ restricts protective innate lymphoid cell group II (ILC2) function in the lung following challenge with the pandemic H1N1 A/CA/04/2009 (CA04) influenza virus. Specifically, IFN-γ deficiency resulted in enhanced ILC2 activity, characterized by increased production of interleukin (IL)-5 and amphiregulin, and improved tissue integrity, yet no change in ILC2 numbers, viral load or clearance. We further found that IFN-γ-deficient mice, as well as wild-type animals treated with neutralizing anti-IFN-γ antibody, exhibited decreased susceptibility to lethal infection with H1N1 CA04 influenza virus, and moreover that survival was dependent on the presence of IL-5. The beneficial effects of IFN-γ neutralization were not observed in ILC2-deficient animals. These data support the novel concept that IFN-γ can have a detrimental role in the pathogenesis of influenza through a restriction in ILC2 activity. Thus, regulation of ILC2 activity is a potential target for post-infection therapy of influenza.
Indexed as
Identifiers
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.