ArticleOtolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery2025
Characterizing the Cellular Constituents of Proximal Airway Disease in Granulomatosis With Polyangiitis.
Article in Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Systemic Immunosuppression to Reduce Surgical Intervention in ANCA-Negative Subglottic Stenosis.The Laryngoscope · 2026Article
- Tracheobronchial Stenosis in Granulomatosis With Polyangiitis: Immunosuppressant Use and Airway Dilation Frequency.ACR open rheumatology · 2026Article
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Authors and funding
10 authors.
Funding
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Abstract
objectiveGranulomatosis with polyangiitis (GPA) is a rare multisystem autoimmune vasculitis. 10-20% of patients suffer life-threatening obstruction of their proximal airways. Although progress has been made in the treatment of systemic disease, ameliorating airway disease in GPA remains an unmet need arising from limited understanding of disease pathogenesis. We sought to characterize the cellular constituents of the affected proximal airway mucosa in GPA airway scar. STUDY
designBasic/translational study.
settingSingle tertiary care center.
methodsUsing single-cell RNA sequencing, we profiled the cellular constituents of proximal airway samples from GPA and disease comparators (GPA; n = 9, idiopathic subglottic stenosis: iSGS; n = 7, post-intubation proximal stenosis: PIPS; n = 5, and control; n = 10). We report transcriptomes for subglottic epithelial, immune, endothelial, and stromal cell types and map expression of GPA risk genes to tissue types present in the proximal airway. We compared differential gene expression across immune cell populations and performed pseudotime analysis using Monocle 3.
resultsSimilar to iSGS and PIPS, the subglottic mucosa of GPA patients demonstrated an abundant immune infiltrate. 71% of the established GPA risk genes (10 of 14) localized to T cells and macrophages. Differential gene expression and pseudotime analysis revealed a sub-population of CD4-/CD8- inflammatory T cells that only originated from GPA.
conclusionWe characterized the cellular composition of GPA airway disease and demonstrated that the expression of GPA risk alleles is predominantly localized to immune cell populations. We also identified a subset of inflammatory T cells that is unique to GPA.
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