ArticleFrontiers in immunology2025
IL-17A drives a fibroblast-neutrophil-NET axis to exacerbate immunopathology in the lung with diffuse alveolar damage.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- The landscape of protein post-translational modifications in the pathogenesis of acute respiratory distress syndrome.Journal of thoracic disease · 2026Review
- Factors associated with circulating levels of IL-17A in a high HIV-burden population.Scientific reports · 2026Article
- Context-specific roles for IL-17 in tuberculosis.PLoS pathogens · 2026Review
- Immune evasion of multidrug-resistant bacteria: insights from lung innate immune cells and targeted therapies.Frontiers in cellular and infection microbiology · 2026Review
- Clinical value of IL-17-targeted intervention in tissue injury repair: from bidirectional mechanisms to therapeutic strategies.Frontiers in immunology · 2026Review
- A thermosensitive hydrogel encapsulating 2-DG alleviates periodontitis by inhibiting glycolysis and effector response of Th17 cells.Frontiers in pharmacology · 2026Article
- Neutrophil extracellular traps in pulmonary fibrosis: mechanisms, immunity and therapeutic targets.Frontiers in immunology · 2026Review
- Dual role of IL-17A in COPD: amplifier of inflammatory cascades and mediator of airway remodeling and alveolar destruction.Frontiers in immunology · 2026Review
- Engineered T cell therapy for the treatment of cardiac fibrosis during chronic phase of myocarditis.Theranostics · 2026Article
- The shifting balance: innate lymphoid cell plasticity in chronic gut diseases.Frontiers in immunology · 2026Review
- Immunopathogenic Mechanisms in Connective Tissue Disease-Associated Interstitial Lung Disease: Incessant Loop of Immunity to Fibrosis.International journal of molecular sciences · 2025Review
- Implicates of PIP5K1α in asthma-related biological processes: insights into mechanisms and therapeutic potential.Journal of translational medicine · 2025Review
- MASLD Exacerbates Chronic Low-dose PMIn vivo (Athens, Greece)Article
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Authors and funding
9 authors.
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Abstract
Diffuse alveolar damage (DAD), a lethal manifestation of acute lung injury, remains a critical public health concern due to the absence of targeted therapies. However, the underlying cellular and molecular mechanisms responsible for immunopathology during DAD progression are largely undefined. Here, by integrating single cell RNA sequencing, functional assays, and genetic/pharmacological interventions in a mouse model of ricin-induced DAD, we revealed a significant accumulation of neutrophil with an activated phenotype that plays a critical role in immunopathology. We observed the formation of neutrophil extracellular traps (NETs) during DAD, which further intensified inflammation and tissue injury. IL-17A signaling activity was upregulated in DAD-affected lungs, while IL-17A deficiency or functional blockade significantly attenuated neutrophil recruitment, NET generation, and tissue damage. Mechanically, IL-17A stimulates lung resident fibroblasts to produce the neutrophil chemoattractant CXCL1. Notably, type 3 innate lymphoid cells (ILC3) emerged as the dominant source of IL-17A, highlighting a triad of interactions among ILC3, fibroblast, and neutrophil in DAD pathogenesis. This finding delineates a pathogenic IL-17A-neutrophil-NET axis that amplifies lung immunopathology after ricin-induced DAD, a deeper understanding of these relationships may pave the way for mitigate DAD immunopathology and other lung inflammatory disorders.
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