ArticleThe Journal of allergy and clinical immunology2022
TLR3-driven IFN-β antagonizes STAT5-activating cytokines and suppresses innate type 2 response in the lung.
Article in The Journal of allergy and clinical immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The trial behind it
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Who cites it
12 citing papers in PubMed, 9 citations in OpenAlex.
- Stem cell factor 248 shapes ILC2 transcriptional programs and promotes mucosal inflammation in allergic asthma.Frontiers in immunology · 2026Article
- Skin-lung axis in the atopic march: The immune link from skin to lungs.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Update on type 2 immunity.The Journal of allergy and clinical immunology · 2025Review
- Role of toll-like receptors in pulmonary immunity: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Molecular mechanisms regulating T helper 2 cell differentiation and function.Current opinion in immunology · 2024Review
- ATF3 coordinates the survival and proliferation of cardiac macrophages and protects against ischemia-reperfusion injury.Nature cardiovascular research · 2024Article
- The modulation of pulmonary group 2 innate lymphoid cell function in asthma: from inflammatory mediators to environmental and metabolic factors.Experimental & molecular medicine · 2023Review
- Interferons as negative regulators of ILC2s in allergic lung inflammation and respiratory viral infections.Journal of molecular medicine (Berlin, Germany) · 2023Review
- The Functional Role of Group 2 Innate Lymphoid Cells in Asthma.Biomolecules · 2023Review
- Metabolic regulation by prostaglandin EAllergy · 2023Article
- Allergen-induced DNA release by the airway epithelium amplifies type 2 immunity.The Journal of allergy and clinical immunology · 2023Article
- Innate Immune Responses by Respiratory Viruses, Including Rhinovirus, During Asthma Exacerbation.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGroup 2 innate lymphoid cells (ILC2s) are involved in type 2 immune responses in mucosal organs and are associated with various allergic diseases in humans. Studies are needed to understand the molecules and pathways that control ILC2s.
objectiveThe aims of this study were to develop a mouse model that limits the innate type 2 immune response in the lung and to investigate the immunologic mechanisms involved in regulation of lung ILC2s.
methodsNaive BALB/c mice were administered various Toll-like receptor agonists and exposed intranasally to the fungal allergen Alternaria alternata. The mechanisms were investigated using gene knockout mice as well as cultures of lung cells and isolated lung ILC2s.
resultsPolyinosinic-polycytidylic acid, or poly (I:C), effectively inhibited innate type 2 response to A alternata. Poly (I:C) promoted production of IFNα, -β, and -γ, and its inhibitory effects were dependent on the IFN-α/β receptor pathway. IFN-β was 100 times more potent than IFN-α at inhibiting type 2 cytokine production by lung ILC2s. Signal transducer and activator of transcription 5 (STAT5)-activating cytokines, including IL-2, IL-7, and thymic stromal lymphopoietin, but not IL-33, promoted survival and proliferation of lung ILC2s in vitro, while IFN-β blocked these effects. Expression of the transcription factor GATA3, which is critical for differentiation and maintenance of ILC2s, was inhibited by IFN-β.
conclusionsIFN-β blocks the effects of STAT5-activating cytokines on lung ILC2s and inhibits their survival and effector functions. Administration of IFN-β may provide a new strategy to treat diseases involving ILC2s.
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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.