ArticleMucosal immunology2018
C3a is required for ILC2 function in allergic airway inflammation.
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 27 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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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Activation of B1 B cells by F. tularensis atypical LPS depends on classical complement and C3a.PLoS pathogens · 2025Article
- Article
- Complement's involvement in allergic Th2 immunity: a cross-barrier perspective.The Journal of clinical investigation · 2025Review
- Th2 predominance and decreased NK cells in patients with hereditary angioedema.Frontiers in immunology · 2025Article
- Complement System and Adhesion Molecule Skirmishes in Fabry Disease: Insights into Pathogenesis and Disease Mechanisms.International journal of molecular sciences · 2024Review
- Airborne indoor allergen serine proteases and their contribution to sensitisation and activation of innate immunity in allergic airway disease.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Lung ILC2s are activated in BALB/c mice born to immunized mothers despite complete protection against respiratory syncytial virus.Frontiers in immunology · 2024Article
- Group 2 Innate Lymphoid Cells in Allergic Rhinitis.Journal of inflammation research · 2024Review
- A computational approach for the identification of key genes and biological pathways of chronic lung diseases: a systems biology approach.BMC medical genomics · 2023Article
- Interorgan communication with the liver: novel mechanisms and therapeutic targets.Frontiers in immunology · 2023Review
- Exacerbated lung inflammation following secondary RSV exposure is CD4+ T cell-dependent and is not mitigated in infant BALB/c mice born to PreF-vaccinated dams.Frontiers in immunology · 2023Article
- Hypoxia induces adrenomedullin from lung epithelia, stimulating ILC2 inflammation and immunity.The Journal of experimental medicine · 2022Article
- Development and function of regulatory innate lymphoid cells.Frontiers in immunology · 2022Review
- Targetable pathogenic mechanisms in nasal polyposis.International forum of allergy & rhinology · 2021Review
- Glucocorticoids and Androgens Protect From Gastric Metaplasia by Suppressing Group 2 Innate Lymphoid Cell Activation.Gastroenterology · 2021Article
- Mesenchymal stem cells regulate type 2 innate lymphoid cells via regulatory T cells through ICOS-ICOSL interaction.Stem cells (Dayton, Ohio) · 2021Article
- Group 2 Innate Lymphoid Cells: Team Players in Regulating Asthma.Annual review of immunology · 2021Article
- IL-10-Producing ILCs: Molecular Mechanisms and Disease Relevance.Frontiers in immunology · 2021Review
- The Role of Type 2 Innate Lymphoid Cells in Allergic Diseases.Frontiers in immunology · 2021Review
- Group 2 Innate Lymphoid Cells Coordinate Damage Response in the Stomach.Gastroenterology · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Aberrant type 2 responses underlie the pathologies in allergic diseases like asthma, yet, our understanding of the mechanisms that drive them remains limited. Recent evidence suggests that dysregulated innate immune factors can perpetuate asthma pathogenesis. In susceptible individuals, allergen exposure triggers the activation of complement, a major arm of innate immunity, leading to the aberrant generation of the C3a anaphylatoxin. C3 and C3a have been shown to be important for the development of Th2 responses, yet remarkably, the mechanisms by which C3a regulates type 2 immunity are relatively unknown. We demonstrate a central role for C3a in driving type 2 innate lymphoid cells (ILC2)-mediated inflammation in response to allergen and IL-33. Our data suggests that ILC2 recruitment is C3a-dependent. Further, we show that ILC2s directly respond to C3a, promoting type 2 responses by specifically: (1) inducing IL-13 and granulocyte-macrophage colony-stimulating factor, whereas inhibiting IL-10 production from ILC2; and (2) enhancing their antigen-presenting capability during ILC-T-cell cross-talk. In summary, we identify a novel mechanism by which C3a can mediate aberrant type 2 responses to aeroallergen exposure, which involves a yet unrecognized cross-talk between two major innate immune components-complement and group 2 innate lymphoid cells.
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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.