ArticleRespiratory research2017
IL-18 associated with lung lymphoid aggregates drives IFNγ production in severe COPD.
Article in Respiratory research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- Migration of immune cells in tumors and inflammation: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Epigenetic dysregulation of IRF9 drives excessive interferon signaling in COPD.EMBO molecular medicine · 2026Article
- CXCL1 augments host defense against Legionella pneumophila through the IL-18-IFN-γ axis and neutrophil homeostasis.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Tertiary Lymphoid Structures Across Organs: Context, Composition, and Clinical Levers.Immunological reviews · 2025Review
- Lymph node or lymphoid aggregate? Impact on cancer resection quality, clinical prognosis, and tumor staging.Histology and histopathology · 2025Review
- IFNγ regulates MR1 transcription and antigen presentation.Frontiers in immunology · 2025Article
- Tertiary lymphoid structures in diseases: immune mechanisms and therapeutic advances.Signal transduction and targeted therapy · 2024Review
- Inflammation as the nexus: exploring the link between acute myocardial infarction and chronic obstructive pulmonary disease.Frontiers in cardiovascular medicine · 2024Review
- Aspirin-triggered resolvin D1 modulates pulmonary and neurological inflammation in an IL-22 knock-out organic dust exposure mouse model.Frontiers in immunology · 2024Article
- Role of tertiary lymphoid organs in the regulation of immune responses in the periphery.Cellular and molecular life sciences : CMLS · 2022Review
- Proteomic analysis in primary T cells reveals IL-7 alters T cell receptor thresholding via CYTIP/cytohesin/LFA-1 localisation and activation.The Biochemical journal · 2022Article
- Hedgehog interacting protein-expressing lung fibroblasts suppress lymphocytic inflammation in mice.JCI insight · 2021Article
- N-Acetylcysteine (NAC) Inhibits Synthesis of IL-18 in Macrophage by Suppressing NLRP3 Expression to Reduce the Production of IFN-Computational and mathematical methods in medicine · 2021Article
- A comprehensive pathway map of IL-18-mediated signalling.Journal of cell communication and signaling · 2020Article
- Innate Lymphoid Cells in the Airways: Their Functions and Regulators.Allergy, asthma & immunology research · 2020Review
- Recent advances in chronic obstructive pulmonary disease pathogenesis: from disease mechanisms to precision medicine.The Journal of pathology · 2020Review
- Role of iBALT in Respiratory Immunity.Current topics in microbiology and immunology · 2020Review
- Serum interleukin-18: A novel prognostic indicator for acute respiratory distress syndrome.Medicine · 2019Article
- Friend or Foe: The Protective and Pathological Roles of Inducible Bronchus-Associated Lymphoid Tissue in Pulmonary Diseases.Journal of immunology (Baltimore, Md. : 1950) · 2019Review
- Review
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIncreased interferon gamma (IFNγ) release occurs in Chronic Obstructive Pulmonary Disease (COPD) lungs. IFNγ supports optimal viral clearance, but if dysregulated could increase lung tissue destruction.
methodsThe present study investigates which mediators most closely correlate with IFNγ in sputum in stable and exacerbating disease, and seeks to shed light on the spatial requirements for innate production of IFNγ, as reported in mouse lymph nodes, to observe whether such microenvironmental cellular organisation is relevant to IFNγ production in COPD lung.
resultsWe show tertiary follicle formation in severe disease alters the dominant mechanistic drivers of IFNγ production, because cells producing interleukin-18, a key regulator of IFNγ, are highly associated with such structures. Interleukin-1 family cytokines correlated with IFNγ in COPD sputum. We observed that the primary source of IL-18 in COPD lungs was myeloid cells within lymphoid aggregates and IL-18 was increased in severe disease. IL-18 released from infected epithelium or from activated myeloid cells, was more dominant in driving IFNγ when IL-18-producing and responder cells were in close proximity.
conclusionsUnlike tight regulation to control infection spread in lymphoid organs, this local interface between IL-18-expressing and responder cell is increasingly supported in lung as disease progresses, increasing its potential to increase tissue damage via IFNγ.
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Registered trials
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