ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Mature cystic fibrosis airway neutrophils suppress T cell function: evidence for a role of arginase 1 but not programmed death-ligand 1.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 72 citations in OpenAlex.
- Patient-centred understanding of quality of life, symptoms, health equity in cystic fibrosis (PULSE-CF): study protocol for an observational study.BMJ open respiratory research · 2026Article
- CFTR modulators exert subset-specific phenotype remodeling on circulating neutrophils in cystic fibrosis.ImmunoHorizons · 2026Article
- From Bone Marrow Reserve to Metastatic Niche: How Neutrophil-Lineage Cells Shape Skeletal Colonization.International journal of molecular sciences · 2026Review
- The single-cell transcriptional landscape of the pediatric cystic fibrosis lung from minimally invasive respiratory specimens.Scientific reports · 2026Article
- Systemic and airway T cell dynamics with influenza-specific immune recovery by cystic fibrosis elexacaftor/tezacaftor/ivacaftor therapy.Respiratory research · 2026Article
- Neutrophil Plasticity in Airway Disease: Balancing Damage and Repair.Journal of innate immunity · 2026Review
- Mechanistic insights into neutrophil involvement in liver transplant ischemia-reperfusion injury and rejection.Frontiers in immunology · 2026Review
- People with cystic fibrosis with high sputum neutrophil elastase on elexacaftor-tezacaftor-ivacaftor exhibit worse pulmonary function and pro-inflammatory airway milieu.Scientific reports · 2025Article
- Early life elevations of methionine oxidation and ornithine track and predict cystic fibrosis structural lung disease.ERJ open research · 2025Article
- Detection of pre-existing immunity to bacterial Cas9 proteins in people with cystic fibrosis.ImmunoHorizons · 2025Article
- Innate Immunity in Cystic Fibrosis: Varied Effects of CFTR Modulator Therapy on Cell-to-Cell Communication.International journal of molecular sciences · 2025Review
- Article
- Regulatory T cells in lung disease and transplantation.Bioscience reports · 2023Review
- Neutrophil swarms containing myeloid-derived suppressor cells are crucial for limiting oral mucosal infection by C. albicans.Research square · 2023Article
- The double-edged role of neutrophil heterogeneity in inflammatory diseases and cancers.MedComm · 2023Review
- Review
- Pulmonary exacerbations in early cystic fibrosis lung disease are marked by strong modulation of CD3 and PD-1 on luminal T cells.Frontiers in immunology · 2023Article
- Interactions between neutrophils and T-helper 17 cells.Frontiers in immunology · 2023Review
- Cystic fibrosis autoantibody signatures associate withFrontiers in immunology · 2023Article
- Inhibition of Recruitment and Activation of Neutrophils by Pyridazinone-Scaffold-Based Compounds.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Bacteria colonize cystic fibrosis (CF) airways, and although T cells with appropriate Ag specificity are present in draining lymph nodes, they are conspicuously absent from the lumen. To account for this absence, we hypothesized that polymorphonuclear neutrophils (PMNs), recruited massively into the CF airway lumen and actively exocytosing primary granules, also suppress T cell function therein. Programmed death-ligand 1 (PD-L1), which exerts T cell suppression at a late step, was expressed bimodally on CF airway PMNs, delineating PD-L1(hi) and PD-L1(lo) subsets, whereas healthy control (HC) airway PMNs were uniformly PD-L1(hi). Blood PMNs incubated in CF airway fluid lost PD-L1 over time; in coculture, Ab blockade of PD-L1 failed to inhibit the suppression of T cell proliferation by CF airway PMNs. In contrast with PD-L1, arginase 1 (Arg1), which exerts T cell suppression at an early step, was uniformly high on CF and HC airway PMNs. However, arginase activity was high in CF airway fluid and minimal in HC airway fluid, consistent with the fact that Arg1 activation requires primary granule exocytosis, which occurs in CF, but not HC, airway PMNs. In addition, Arg1 expression on CF airway PMNs correlated negatively with lung function and positively with arginase activity in CF airway fluid. Finally, combined treatment with arginase inhibitor and arginine rescued the suppression of T cell proliferation by CF airway fluid. Thus, Arg1 and PD-L1 are dynamically modulated upon PMN migration into human airways, and, Arg1, but not PD-L1, contributes to early PMN-driven T cell suppression in CF, likely hampering resolution of infection and inflammation.
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