ArticleTransplantation2019
IL-17A Contributes to Lung Fibrosis in a Model of Chronic Pulmonary Graft-versus-host Disease.
Article in Transplantation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
What it found
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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
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- A Review of CXCL1 in Cardiac Fibrosis.Frontiers in cardiovascular medicine · 2021Pooled it
- Chronic Graft-versus-host Disease, Part 1: How Preclinical Models Shape Our Understanding of Biology and Pave the Way for Future Therapeutic Interventions.Transplantation · 2025Review
- Persistent and progressive acute lung allograft dysfunction is linked to cell compositional and transcriptional changes in small airways.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2025Article
- IL-17A-Induced Redox Imbalance and Inflammatory Responses in Mice Lung via Act1-TRAF6-IKBα Signaling Pathway: Implications for Lung Disease Pathogenesis.Inflammation · 2025Article
- Rifaximin ameliorates influenza A virus infection-induced lung barrier damage by regulating gut microbiota.Applied microbiology and biotechnology · 2024Article
- Cellular and Molecular Genetic Mechanisms of Lung Fibrosis Development and the Role of Vitamin D: A Review.International journal of molecular sciences · 2024Review
- The role and therapeutic targeting of the CCL2/CCR2 signaling axis in inflammatory and fibrotic diseases.Frontiers in immunology · 2024Review
- αPD-1 immunotherapy promotes IL-17A production and promotes the formation of acute radiation-induced lung injury.American journal of cancer research · 2024Article
- Donor IL-17 receptor A regulates LPS-potentiated acute and chronic murine lung allograft rejection.JCI insight · 2023Article
- IL-17A neutralization fails to attenuate airway remodeling and potentiates a proinflammatory lung microenvironment in diacetyl-exposed rats.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Inflammogenic effect of polyacrylic acid in rat lung following intratracheal instillation.Particle and fibre toxicology · 2022Article
- The role of PD-1/PD-L1 axis in idiopathic pulmonary fibrosis: Friend or foe?Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundChronic pulmonary graft-versus-host disease (cpGVHD) after hematopoietic cell transplant (HCT) manifests as progressive airway and parenchymal lung fibrosis. On the basis of our prior data, mice that undergo allogeneic HCT with Tbet-knockout donors (AlloTbet) have increased lung Th17 cells and IL-17A and develop fibrosis resembling human cpGVHD. The role of IL-17A in posttransplant pulmonary fibrosis remains incompletely understood. We hypothesized that IL-17A is necessary for development of murine cpGVHD in this model.
methodsAlloTbet mice received weekly intraperitoneal anti-IL-17A or IgG (200 μg/mouse) starting 2 weeks post-HCT and were sacrificed after week 5. Histologic airway and parenchymal fibrosis were semiquantitatively graded in a blinded fashion. Lung cells and proteins were measured by flow cytometry, ELISA, and multicytokine assays.
resultsAnti-IL-17A modestly decreased airway and parenchymal lung fibrosis, along with a striking reduction in pulmonary neutrophilia, IL-6, MIP-1α, MIP-1β, CXCL1, and CXCL5 in AlloTbet mice. Additionally, anti-IL-17A decreased CCL2, inflammatory monocytes and macrophages, and Th17 cells.
conclusionsIn the setting of murine AlloHCT with Tbet donors, IL-17A blockade decreases fibrotic features of cpGVHD. This may be mediated by the observed reduction in neutrophils or specific lung monocyte and macrophage populations or alternatively via a direct effect on fibroblasts. Collectively, our results further suggest that anti-IL-17A strategies could prove useful in preventing alloimmune-driven fibrotic lung diseases.
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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.