ArticleRespiratory research2015
Lymphocyte senescence in COPD is associated with decreased histone deacetylase 2 expression by pro-inflammatory 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 19 papers.
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Who cites it
19 citing papers in PubMed, 40 citations in OpenAlex.
- Immunoinflammation and post-translational modifications in the aging process.Journal of translational medicine · 2025Review
- Immunosenescence and Inflammation in Chronic Obstructive Pulmonary Disease: A Systematic Review.Journal of clinical medicine · 2024Review
- Aging and aging-related diseases: from molecular mechanisms to interventions and treatments.Signal transduction and targeted therapy · 2022Review
- Inclusion Body Myositis and Neoplasia: A Narrative Review.International journal of molecular sciences · 2022Review
- 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
- Age-associated phenotypic imbalance in TCD4 and TCD8 cell subsets: comparison between healthy aged, smokers, COPD patients and young adults.Immunity & ageing : I & A · 2022Article
- The mechanistic role of neutrophil lymphocyte ratio perturbations in the leading non communicable lifestyle diseases.F1000Research · 2022Review
- Mechanisms, Pathophysiology and Currently Proposed Treatments of Chronic Obstructive Pulmonary Disease.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Article
- Preclinical and clinical progress for HDAC as a putative target for epigenetic remodeling and functionality of immune cells.International journal of biological sciences · 2021Review
- Therapeutic Targeting Steroid Resistant Pro-Inflammatory NK and NKT-Like Cells in Chronic Inflammatory Lung Disease.International journal of molecular sciences · 2019Review
- Genetic ablation of histone deacetylase 2 leads to lung cellular senescence and lymphoid follicle formation in COPD/emphysema.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Aminophylline restores glucocorticoid sensitivity in a guinea pig model of sudden sensorineural hearing loss induced by lipopolysaccharide.Scientific reports · 2017Article
- HDAC4 is expressed on multiple T cell lineages but dispensable for their development and function.Oncotarget · 2017Article
- Emerging pharmaceutical therapies for COPD.International journal of chronic obstructive pulmonary disease · 2017Review
- Steroid resistance in COPD is associated with impaired molecular chaperone Hsp90 expression by pro-inflammatory lymphocytes.Respiratory research · 2016Article
- Steroid Resistant CD8Frontiers in immunology · 2016Review
- Lymphocyte senescence in COPD is associated with decreased sirtuin 1 expression in steroid resistant pro-inflammatory lymphocytes.Therapeutic advances in respiratory diseaseArticle
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHistone acetyltransferases (HAT) and histone deacetylases (HDAC) are enzymes that upregulate and down-regulate pro-inflammatory gene transcription respectively. HDAC2 is required by corticosteroids to switch off activated inflammatory genes and is reduced in lung macrophages in COPD. We have shown that COPD patients have increased steroid resistant CD28null (senescent) pro-inflammatory T and NKT-like peripheral blood cells (particularly CD8+ subsets) and we hypothesized that these changes would be associated with a loss of HDAC2 from these senescent pro-inflammatory lymphocytes.
methodsBlood was collected from 10 COPD and 10 aged-matched controls. Intracellular pro-inflammatory cytokines, IFNγ and TNFα, and expression of CD28, HDAC2 and HAT, were determined in lymphocyte subsets in the presence of ± 5 mg/ml theophylline (HDAC2 activator), 10 μM prednisolone and 2.5 ng/ml cyclosporine A (immunosuppressant), using flow cytometry.
resultsThere was a loss of HDAC2 from CD28null CD8+ T and NKT-like cells in COPD. There was a significant negative correlation between HDAC2 expression and the percentage of CD28null CD8+ T and NKT-like cells producing IFNγ or TNFα in all subjects (eg, COPD: R = -.763, p < 0.001 for T-cell IFNγ). There was a synergistic upregulation of HDAC2 and associated decrease in pro-inflammatory cytokine production in CD28nullCD8+ T and NKT-like cells in the presence of 5 mg/L theophylline + 10(-6) M prednisolone or 2.5 ng/mL cyclosporine A (CsA).
conclusionsLymphocyte senescence in COPD is associated with loss of HDAC2 in CD28nullCD8+ T and NKT-like cells. Alternative treatment options such as combined theophylline with low-dose CsA, that inhibit these pro-inflammatory cells, may reduce systemic inflammation in COPD.
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