ArticleEnvironmental toxicology2024
Blocking IL-23 Signaling Mitigates Cigarette Smoke-Induced Murine Emphysema.
Article in Environmental toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Interleukin-23 in lung and airway diseases: from pathogenesis to precision-guided therapeutic targeting.Frontiers in pharmacology · 2026Review
- Emerging role of small RNAs in inflammatory bowel disease and associated colorectal cancer (Review).International journal of molecular medicine · 2025Review
- Elevated Th1 and terminally differentiated cytotoxic T cells with suppressed Tc17 lymphocytes in lung tissue of advanced COPD and IPF patients undergoing lung transplantation.Frontiers in immunology · 2025Article
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Authors and funding
5 authors.
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Abstract
Inflammatory cell infiltration is a characteristic feature of COPD and correlates directly with the severity of the disease. Interleukin-23 (IL-23) is a pro-inflammatory cytokine that regulates Th-17 inflammation, which mediates many pathophysiological events in COPD. The primary goal of this study was to determine the role of IL-23 as a mediator of key pathologic processes in cigarette smoke-induced COPD. In this study, we report an increase in IL23 gene expression in the lung biopsies of COPD patients compared to controls and identified a positive correlation between IL23 gene expression and disease severity. In a cigarette smoke-induced murine emphysema model, the suppression of IL-23 with a monoclonal blocking antibody reduced the severity of cigarette smoke-induced murine emphysema. Mechanistically, the suppression of IL-23 was associated with a reduction in immune cell infiltration, oxidative stress injury, and apoptosis, suggesting a role for IL-23 as an essential immune mediator of the inflammatory processes in the pathogenesis of CS-induced emphysema.
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Registered trials
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