ArticleFrontiers in immunology2021
Cyclic-di-GMP Induces STING-Dependent ILC2 to ILC1 Shift During Innate Type 2 Lung Inflammation.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 23 citations in OpenAlex.
- Innate airway immune response to fungal allergens.Frontiers in immunology · 2026Review
- PM2.5 exacerbates house dust mite-induced allergic rhinitis via STING-mediated nasal epithelial barrier disruption.Frontiers in immunology · 2026Article
- ILC2 Diversity, Location, and Function in Pulmonary Disease.Immunological reviews · 2025Review
- The Importance of Lung Innate Immunity During Health and Disease.Pathogens (Basel, Switzerland) · 2025Review
- Study on the Mechanism of Artesunate in Modulating AR Epithelial Injury and Th2-Type Inflammatory Status.Journal of inflammation research · 2025Article
- PIP-seq identifies novel heterogeneous lung innate lymphocyte population activation after combustion product exposure.Scientific reports · 2024Article
- Cyclic-di-GMP induces inflammation and acute lung injury through direct binding to MD2.Clinical and translational medicine · 2024Article
- The production, function, and clinical applications of IL-33 in type 2 inflammation-related respiratory diseases.Frontiers in immunology · 2024Review
- Interferons as negative regulators of ILC2s in allergic lung inflammation and respiratory viral infections.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Beyond DNA sensing: expanding the role of cGAS/STING in immunity and diseases.Archives of pharmacal research · 2023Review
- ILC1: Development, maturation, and transcriptional regulation.European journal of immunology · 2023Review
- Intranasal immunization with a Bucl8-based vaccine ameliorates bacterial burden and pathological inflammation, and promotes an IgG2a/b dominant response in an outbred mouse model ofFrontiers in immunology · 2023Article
- RAGE contributes to allergen driven severe neutrophilic airway inflammationFrontiers in immunology · 2023Article
- STING Targeting in Lung Diseases.Cells · 2022Review
- Airway administration of OM-85, a bacterial lysate, blocks experimental asthma by targeting dendritic cells and the epithelium/IL-33/ILC2 axis.The Journal of allergy and clinical immunology · 2022Article
- The Interactions Between Autoinflammation and Type 2 Immunity: From Mechanistic Studies to Epidemiologic Associations.Frontiers in immunology · 2022Review
- STING activation in alveolar macrophages and group 2 innate lymphoid cells suppresses IL-33-driven type 2 immunopathology.JCI insight · 2021Article
- Cyclic-di-GMP Induces STING-Dependent ILC2 to ILC1 Shift During Innate Type 2 Lung Inflammation.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Type 2 inflammation is found in most forms of asthma, which may co-exist with recurrent viral infections, bacterial colonization, and host cell death. These processes drive the accumulation of intracellular cyclic-di-nucleotides such as cyclic-di-GMP (CDG). Group 2 innate lymphoid cells (ILC2s) are critical drivers of type 2 lung inflammation during fungal allergen exposure in mice; however, it is unclear how CDG regulates lung ILC responses during lung inflammation. Here, we show that intranasal CDG induced early airway type 1 interferon (IFN) production and dramatically suppressed CD127+ST2+ ILC2s and type 2 lung inflammation during
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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.