ReviewFrontiers in immunology2020
Contributions of IL-33 in Non-hematopoietic Lung Cells to Obstructive Lung Disease.
Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 21 citations in OpenAlex.
- A multifunctional ICAM1-directed MnO₂@ZIF8 nanoplatform with Tanshinone IIA synergistically reverses senescence and restores alveolar regeneration in septic lung injury.Journal of nanobiotechnology · 2026Article
- GATA2 controls alveolar macrophage inflammatory gene expression and metabolic function.JCI insight · 2026Article
- Chronic IL-21 exposure reshapes pulmonary environment, elevating risk of respiratory diseases.Cellular and molecular life sciences : CMLS · 2026Article
- The Major Role of Type 2 Inflammation in Asthma: From the Perspective of Immunological Mechanism.BioMed research international · 2026Review
- Beyond inhaled medications: precision medicine and biologic therapies targeting the IL-33/TSLP/type 2 axis in COPD.Frontiers in immunology · 2026Review
- Safety Profile of Tozorakimab (an Anti-IL-33 Monoclonal Antibody): Data from the FRONTIER Phase 2 Program.Biologics : targets & therapy · 2026Article
- Tropisetron Suppresses Chronic Pancreatitis and Pancreatic Cancer by Blocking Interleukin 33 Expression.Cancers · 2025Article
- Review
- The epithelial era of asthma research: knowledge gaps and future direction for patient care.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Eosinophil-Epithelial Cell Interactions in Asthma.International archives of allergy and immunology · 2024Review
- Analysis of Key Genes and miRNA-mRNA Networks Associated with Glucocorticoids Treatment in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2024Article
- Review
- Airway Wall Remodeling in Childhood Asthma-A Personalized Perspective from Cell Type-Specific Biology.Journal of personalized medicine · 2021Review
- IL-33 in Rheumatic Diseases.Frontiers in medicine · 2021Review
- Interleukin-33/ Suppression of Tumorigenicity 2 in Renal Fibrosis: Emerging Roles in Prognosis and Treatment.Frontiers in physiology · 2021Review
- Generation and Characterization of Torudokimab (LY3375880): A Monoclonal Antibody That Neutralizes Interleukin-33.Journal of inflammation research · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Interleukin (IL)-33 plays important roles in pulmonary immune responses and lung diseases including asthma and chronic obstructive pulmonary disease (COPD). There is substantial interest in identifying and characterizing cellular sources vs. targets of IL-33, and downstream signaling pathways involved in disease pathophysiology. While epithelial and immune cells have largely been the focus, in this review, we summarize current knowledge of expression, induction, and function of IL-33 and its receptor ST2 in non-hematopoietic lung cells in the context of health and disease. Under basal conditions, epithelial cells and endothelial cells are thought to be the primary resident cell types that express high levels of IL-33 and serve as ligand sources compared to mesenchymal cells (smooth muscle cells and fibroblasts). Under inflammatory conditions, IL-33 expression is increased in most non-hematopoietic lung cells, including epithelial, endothelial, and mesenchymal cells. In comparison to its ligand, the receptor ST2 shows low expression levels at baseline but similar to IL-33, ST2 expression is upregulated by inflammation in these non-hematopoietic lung cells which may then participate in chronic inflammation both as sources and autocrine/paracrine targets of IL-33. Downstream effects of IL-33 may occur via direct receptor activation or indirect interactions with the immune system, overall contributing to lung inflammation, airway hyper-responsiveness and remodeling (proliferation and fibrosis). Accordingly from a therapeutic perspective, targeting IL-33 and/or its receptor in non-hematopoietic lung cells becomes relevant.
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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.