ArticlePloS one2015
Effect of JAK Inhibitors on Release of CXCL9, CXCL10 and CXCL11 from Human Airway Epithelial Cells.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 69 citations in OpenAlex.
- LncRNA AFAP1-AS1 mediates therapy-dependent expression of CCL5, CXCL10 and MMP9 in multiple sclerosis.Biochemistry and biophysics reports · 2026Article
- ZBTB7B inhibits glioma tumorigenicity by upregulating GPR17 and CXCL10.Journal of molecular cell biology · 2026Article
- Activation of STAT3 in the COPD airway epithelium.ERJ open research · 2026Article
- CXCL11 levels regulate lung Treg responses to deter the onset of HIV-related COPD.Respiratory research · 2026Article
- A cell line-derived, immune-competent neurospheroid model to study neuroinflammation and human brain disorders.Frontiers in immunology · 2026Article
- Interleukin-23 in lung and airway diseases: from pathogenesis to precision-guided therapeutic targeting.Frontiers in pharmacology · 2026Review
- Epithelial Ikkβ deletion modulates immune responses and the IFNγ/CXCL9 axis during early esophageal carcinogenesis.Carcinogenesis · 2025Article
- Development of DPP-4-resistant CXCL9-Fc and CXCL10-Fc chemokines for effective cancer immunotherapy.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Plasma Levels of CXCL9 and MCP-3 are Increased in Asthma-COPD Overlap (ACO) Patients.International journal of chronic obstructive pulmonary disease · 2025Article
- Multi-System-Level Analysis with RNA-Seq on Pterygium Inflammation Discovers Association between Inflammatory Responses, Oxidative Stress, and Oxidative Phosphorylation.International journal of molecular sciences · 2024Article
- PD-1 and CTLA-4 serve as major gatekeepers for effector and cytotoxic T-cell potentiation by limiting a CXCL9/10-CXCR3-IFNγ positive feedback loop.Frontiers in immunology · 2024Article
- Coexpression of PD-L1/PD-1 with CXCR3/CD36 and IL-19 Increase in Extranodal Lymphoma.Journal of immunology research · 2023Article
- Anti-HPV16 oncoproteins siRNA therapy for cervical cancer using a novel transdermal peptide PKU12.Frontiers in oncology · 2023Article
- Interfering with interferons: targeting the JAK-STAT pathway in complications of systemic juvenile idiopathic arthritis (SJIA).Rheumatology (Oxford, England) · 2022Review
- Mechanistic studies of MALAT1 in respiratory diseases.Frontiers in molecular biosciences · 2022Review
- Sputum Cytokine Profiling in COPD: Comparison Between Stable Disease and Exacerbation.International journal of chronic obstructive pulmonary disease · 2022Article
- A New Inflammation-Related Risk Model for Predicting Hepatocellular Carcinoma Prognosis.BioMed research international · 2022Article
- Review
- Article
- The Hidden Burden of Severe Asthma: From Patient Perspective to New Opportunities for Clinicians.Journal of clinical medicine · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCD8+ T-cells are located in the small airways of COPD patients and may contribute to pathophysiology. CD8+ cells express the chemokine receptor, CXCR3 that binds CXCL9, CXCL10 and CXCL11, which are elevated in the airways of COPD patients. These chemokines are released from airway epithelial cells via activation of receptor associated Janus kinases (JAK). This study compared the efficacy of two structurally dissimilar pan-JAK inhibitors, PF956980 and PF1367550, and the glucocorticosteroid dexamethasone, in BEAS-2B and human primary airway epithelial cells from COPD patients and control subjects.
methodsCells were stimulated with either IFNγ alone or with TNFα, and release of CXCL9, CXCL10 and CXCL11 measured by ELISA and expression of CXCL9, CXCL10 and CXCL11 by qPCR. Activation of JAK signalling was assessed by STAT1 phosphorylation and DNA binding.
resultsThere were no differences in the levels of release of CXCL9, CXCL10 and CXCL11 from primary airway epithelial cells from any of the subjects or following stimulation with either IFNγ alone or with TNFα. Dexamethasone did not inhibit CXCR3 chemokine release from stimulated BEAS-2B or primary airway epithelial cells. However, both JAK inhibitors suppressed this response with PF1367550 being ~50-65-fold more potent than PF956980. The response of cells from COPD patients did not differ from controls with similar responses regardless of whether inhibitors were added prophylactically or concomitant with stimuli. These effects were mediated by JAK inhibition as both compounds suppressed STAT1 phosphorylation and DNA-binding of STAT1 and gene transcription.
conclusionsThese data suggest that the novel JAK inhibitor, PF1367550, is more potent than PF956980 and that JAK pathway inhibition in airway epithelium could provide an alternative anti-inflammatory approach for glucocorticosteroid-resistant diseases including COPD.
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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.