ArticleFrontiers in immunology2025
Defining a non-eosinophilic inflammatory subtype in COPD: the role of CXCL9 and type 1 immune responses.
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 3 papers.
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Who cites it
3 citing papers in PubMed.
- Qingre Runzao oral liquid and its key compound ophiopogonin D inhibit CXCL9 and block CXCL9/CXCR3 axis to ameliorate asthma by suppressing RAS/ERK pathway.Respiratory research · 2026Article
- Large-scale proteome profiling identifies circulating biomarkers for disease activity and organ involvement in ANCA-associated vasculitides.Frontiers in immunology · 2026Article
- Divergent roles of serum CXCL9 as a biomarker in ILD and COPD: a comparative study.Frontiers in pharmacology · 2026Article
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6 authors.
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Abstract
Background: C-X-C motif chemokine ligand 9 (CXCL9) is induced by the interferon-γ response, and its receptor, C-X-C motif chemokine receptor 3, is a well-established marker of T-helper 1 (Th1) cells, which play an essential role in type 1 immune responses. CXCL9 expression is upregulated in patients with interstitial lung disease (ILD), COVID-19, and asthma. Although type 1 inflammation and CD8 Methods: We conducted a retrospective cohort study. The serum levels of CXCL9, surfactant protein A (SP-A), Krebs von den Lungen-6 (KL-6), and C-reactive protein (CRP) were analyzed in 165 patients with ILD and COPD. COPD was diagnosed using pulmonary function tests according to the Global Initiative for Chronic Obstructive Lung Disease criteria. Statistical analyses included Fisher's exact test, Steel-Dwass test, Mann-Whitney Results: CXCL9 levels were significantly higher in patients with COPD and interstitial ILD than in healthy smokers and non-smokers. The median serum CXCL9 levels in patients with ILD, COPD, healthy smokers, and healthy nonsmokers were 61.6, 69.3, 37.0, and 32.5pg/mL, respectively. CXCL9 levels in patients with COPD significantly correlated with KL-6, SP-A, blood eosinophil ratio, lactate dehydrogenase (LDH), and CRP levels, with correlation coefficients of 0.243, 0.381, 0.225, 0.369, and 0.293, respectively. Additionally, CXCL9 levels were negatively correlated with FEV Conclusions: Our results highlight the potential role of CXCL9 in the inflammatory pathophysiology of COPD.
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