ArticleMucosal immunology2022
Adenosine restrains ILC2-driven allergic airway inflammation via A2A receptor.
Article in Mucosal immunology, 2022. 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 12 papers.
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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.
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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
12 citing papers in PubMed, 22 citations in OpenAlex.
- Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026Review
- Immunomodulatory supramolecular hydrogel for rheumatoid arthritis management via adenosine A2A receptor-mediated macrophage remodeling.Bioactive materials · 2026Article
- ILC2 Diversity, Location, and Function in Pulmonary Disease.Immunological reviews · 2025Review
- Immunomodulatory roles of butyrate in asthma: mechanisms and therapeutic potentials.Frontiers in immunology · 2025Review
- Tissue microenvironment induces tissue specificity of ILC2.Cell death discovery · 2024Review
- The production, function, and clinical applications of IL-33 in type 2 inflammation-related respiratory diseases.Frontiers in immunology · 2024Review
- Ecto-5'-nucleotidase (CD73): an emerging role as prognostic factor in allergic sensitization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Pharmacology of Adenosine Receptors: Recent Advancements.Biomolecules · 2023Review
- CD90 is not constitutively expressed in functional innate lymphoid cells.Frontiers in immunology · 2023Article
- Extracellular Vesicles Derived from Allergen Immunotherapy-Treated Mice Suppressed IL-5 Production from Group 2 Innate Lymphoid Cells.Pathogens (Basel, Switzerland) · 2022Article
- Roles of type 1 regulatory T (Tr1) cells in allergen-specific immunotherapy.Frontiers in allergy · 2022Review
- Neural regulation of ILC2s in allergic airway inflammation.Frontiers in allergy · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although group 2 Innate Lymphoid Cells (ILC2s) play important roles in driving the pathogenesis of allergic airway inflammation, the molecular mechanisms regulating ILC2 responses remain to be fully elucidated. Adenosine signaling is emerging as an important factor to limit excessive inflammation and tissue damage, its role in ILC2-driven airway inflammation remains to be understood. Here we identify adenosine as a negative regulator of ILC2s and allergic airway inflammation. Elevation of adenosine was observed in lungs after protease papain challenge. Adenosine receptor A2A was abundantly expressed in lung ILC2s. The adenosine analog NECA significantly suppress ILC2s responses and relieved airway inflammation induced by IL-33 or papain. Conversely, blockage of adenosine synthesis by CD73 inhibitor APCP or deficiency of A2A aggravated murine airway inflammation. Adoptive transfer of ILC2s into immunodeficiency NCG mice demonstrated that the regulation of ILC2 by adenosine was cell intrinsic. Mechanistic studies showed that the effects of adenosine on ILC2s were associated with changes in transcriptional profiling, and the elevation of intracellular cAMP and resulted NF-κB downregulation. These observations indicate that adenosine-A2A signaling is a negative regulator of ILC2s, which confers protection against airway inflammation and represents a novel therapeutic target for controlling asthma.
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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.