ArticleRespiratory research2015
Lymphocyte senescence in COPD is associated with loss of glucocorticoid receptor expression by pro-inflammatory/cytotoxic lymphocytes.
Article in Respiratory research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 38 citations in OpenAlex.
- Identification of immunogenic cell death-related prognostic genes in gastric cancer.Journal of gastrointestinal oncology · 2026Article
- Targeting immunosenescence in lung diseases: mechanistic insights and clinical interventions.BMC medicine · 2026Review
- Exploring the Interplay between Cellular Senescence, Immunity, and Fibrosing Interstitial Lung Diseases: Challenges and Opportunities.International journal of molecular sciences · 2024Review
- Immunosenescence and Inflammation in Chronic Obstructive Pulmonary Disease: A Systematic Review.Journal of clinical medicine · 2024Review
- Association of lymphocyte subsets and cytokines with bone metabolism: a retrospective, cross-sectional study.BMC musculoskeletal disorders · 2024Article
- The aging lung: microenvironment, mechanisms, and diseases.Frontiers in immunology · 2024Review
- Analysis of Key Genes and miRNA-mRNA Networks Associated with Glucocorticoids Treatment in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2024Article
- Senescence: Pathogenic Driver in Chronic Obstructive Pulmonary Disease.Medicina (Kaunas, Lithuania) · 2022Review
- COPD is associated with increased pro-inflammatory CD28null CD8 T and NKT-like cells in the small airways.Clinical and experimental immunology · 2022Article
- The mechanistic role of neutrophil lymphocyte ratio perturbations in the leading non communicable lifestyle diseases.F1000Research · 2022Review
- Accumulation of CD28Biomolecules · 2021Review
- Use of immune checkpoint inhibitors in cancer patients with pre-existing sarcoidosis.Immunotherapy · 2021Article
- Programmed Cell Death Pathways in the Pathogenesis of Idiopathic Inflammatory Myopathies.Frontiers in immunology · 2021Review
- Article
- Targeting Cell Senescence for the Treatment of Age-Related Bone Loss.Current osteoporosis reports · 2019Review
- Therapeutic Targeting Steroid Resistant Pro-Inflammatory NK and NKT-Like Cells in Chronic Inflammatory Lung Disease.International journal of molecular sciences · 2019Review
- Environmental Exposures and Asthma Development: Autophagy, Mitophagy, and Cellular Senescence.Frontiers in immunology · 2019Review
- Disease- and treatment-associated acquired glucocorticoid resistance.Endocrine connections · 2018Review
- Novel role for receptor dimerization in post-translational processing and turnover of the GRα.Scientific reports · 2018Article
- Progressive slowdown/prevention of cellular senescence by CD9-targeted delivery of rapamycin using lactose-wrapped calcium carbonate nanoparticles.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlucocorticoid (GC) resistance is a major barrier in COPD treatment. We have shown increased expression of the drug efflux pump, Pgp1 in cytotoxic/pro-inflammatory lymphocytes in COPD. Loss of lymphocyte co-stimulatory molecule CD28 (lymphocyte senescence) was associated with a further increase in their pro-inflammatory/cytotoxic potential and resistance to GC. We hypothesized that lymphocyte senescence and increased Pgp1 are also associated with down-regulation of the GC receptor (GCR).
methodsBlood was collected from 10 COPD and 10 healthy aged-matched controls. Flow cytometry was applied to assess intracellular pro-inflammatory cytokines, CD28, Pgp1, GCR, steroid binding and relative cytoplasm/nuclear GCR by CD28+ and CD28null T, NKT-like cells. GCR localization was confirmed by fluorescent microscopy.
resultsCOPD was associated with increased numbers of CD28nullCD8+ T and NKT-like cells. Loss of CD28 was associated with an increased percentage of T and NKT-like cells producing IFNγ or TNFα and associated with a loss of GCR and Dex-Fluor staining but unchanged Pgp1. There was a significant loss of GCR in CD8 + CD28null compared with CD8 + CD28+ T and NKT-like cells from both COPD and controls (eg, mean ± SEM 8 ± 3% GCR + CD8 + CD28null T-cells vs 49 ± 5% GCR + CD8 + CD28+ T-cells in COPD). There was a significant negative correlation between GCR expression and IFNγ and TNFα production by T and NKT-like cells(eg, COPD: T-cell IFNγ R = -.615; ) and with FEV1 in COPD (R = -.777).
conclusionsCOPD is associated with loss of GCR in senescent CD28null and NKT-like cells suggesting alternative treatment options to GC are required to inhibit these pro-inflammatory/cytotoxic cells.
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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.