ArticleAmerican journal of respiratory cell and molecular biology2017
IFN-γ Blocks Development of an Asthma Phenotype in Rhinovirus-Infected Baby Mice by Inhibiting Type 2 Innate Lymphoid Cells.
Article in American journal of respiratory cell and molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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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
40 citing papers in PubMed, 58 citations in OpenAlex.
- Pulmonary Innate Lymphoid Cell Responses during Rhinovirus-induced Asthma ExacerbationsAmerican journal of respiratory and critical care medicine · 2021Trial
- Innate Lymphoid Cells Activation and Transcriptomic Changes in Response to Human Dengue Infection.Frontiers in immunology · 2021Trial
- Androgens protect ILC2S from functional suppression during influenza virus infection.Mucosal immunology · 2026Article
- The IL-33-ILC2 axis: a key regulator of type 2 immunity in respiratory disease.Frontiers in immunology · 2026Review
- ILC2 Diversity, Location, and Function in Pulmonary Disease.Immunological reviews · 2025Review
- The role of innate immune system in respiratory viral infection related asthma.Frontiers in cellular and infection microbiology · 2025Review
- Tuft cell cysteinyl leukotrienes are necessary for rhinovirus-induced mucus metaplasia, type 2 inflammation and airway hyperresponsiveness in immature mice.Frontiers in immunology · 2025Article
- Trained immunity of intestinal tuft cells during infancy enhances host defense against enteroviral infections in mice.EMBO molecular medicine · 2024Article
- Stem cells, Notch-1 signaling, and oxidative stress: a hellish trio in cancer development and progression within the airways. Is there a role for natural compounds?Carcinogenesis · 2024Review
- Tissue-specific features of innate lymphoid cells in antiviral defense.Cellular & molecular immunology · 2024Review
- Early-life pulmonary viral infection leads to long-term functional and lower airway structural changes in the lungs.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Interferons as negative regulators of ILC2s in allergic lung inflammation and respiratory viral infections.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Tissue-resident immunity in the lung: a first-line defense at the environmental interface.Seminars in immunopathology · 2022Review
- Interferon gamma constrains type 2 lymphocyte niche boundaries during mixed inflammation.Immunity · 2022Article
- Interferon-Disease markers · 2022Article
- Neonatal Immune Responses to Respiratory Viruses.Frontiers in immunology · 2022Review
- Innate Immune Responses by Respiratory Viruses, Including Rhinovirus, During Asthma Exacerbation.Frontiers in immunology · 2022Review
- M2 Macrophages promote IL-33 expression, ILC2 expansion and mucous metaplasia in response to early life rhinovirus infections.Frontiers in immunology · 2022Article
- The Promising Effects of Astaxanthin on Lung Diseases.Advances in nutrition (Bethesda, Md.) · 2021Review
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Early-life wheezing-associated infections with rhinovirus (RV) have been associated with asthma development in children. We have shown that RV infection of 6-day-old mice induces mucous metaplasia and airways hyperresponsiveness, which is dependent on IL-13, IL-25, and type 2 innate lymphoid cells (ILC2s). Infection of immature mice fails to induce lung IFN-γ expression, in contrast to mature 8-week-old mice with a robust IFN-γ response, consistent with the notion that deficient IFN-γ production in immature mice permits RV-induced type 2 immune responses. We therefore examined the effects of intranasal IFN-γ administration on RV-induced ILC2 expansion and IL-13 expression in 6-day-old BALB/c and IL-13 reporter mice. Airway responses were assessed by histology, immunofluorescence microscopy, quantitative polymerase chain reaction, ELISA, and flow cytometry. Lung ILC2s were also treated with IFN-γ ex vivo. We found that, compared with untreated RV-infected immature mice, IFN-γ treatment attenuated RV-induced IL-13 and Muc5ac mRNA expression and mucous metaplasia. IFN-γ also reduced ILC2 expansion and the percentage of IL-13-secreting ILC2s. IFN-γ had no effect on the mRNA or protein expression of IL-25, IL-33, or thymic stromal lymphoprotein. Finally, IFN-γ treatment of sorted ILC2s reduced IL-5, IL-13, IL-17RB, ST2, and GATA-3 mRNA expression. We conclude that, in immature mice, IFN-γ inhibits ILC2 expansion and IL-13 expression in vivo and ex vivo, thereby attenuating RV-induced mucous metaplasia. These findings demonstrate the antagonistic function of IFN-γ on ILC2 expansion and gene expression, the absence of which may contribute to the development of an asthma-like phenotype after early-life RV infection.
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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.