ArticleScientific reports2020
Th17/Treg imbalance in COPD development: suppressors of cytokine signaling and signal transducers and activators of transcription proteins.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- AhR as a Common Denominator in Immunity and Inflammation in Chronic Lung Diseases: Molecular and Clinical Insights.Diseases (Basel, Switzerland) · 2026Review
- Dual role of IL-17A in COPD: amplifier of inflammatory cascades and mediator of airway remodeling and alveolar destruction.Frontiers in immunology · 2026Review
- Novel insights into the ROCK-JAK-STAT signaling pathway in upper respiratory tract infections and neurodegenerative diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Cigarette smoke exposure triggers dendritic cell-derived exosome-mediated Th17 and Treg polarization through an autophagy- and necroptosis-associated SIRT1-dependent mechanism in vitro.Frontiers in immunology · 2025Article
- Smoking and osteoimmunology: Understanding the interplay between bone metabolism and immune homeostasis.Journal of orthopaedic translation · 2024Review
- Role of Th17 cells, Treg cells, and Th17/Treg imbalance in immune homeostasis disorders in patients with chronic obstructive pulmonary disease.Immunity, inflammation and disease · 2023Review
- Circadian clock-based therapeutics in chronic pulmonary diseases.Trends in pharmacological sciences · 2022Review
- Cigarette Smoke and Morphine Promote Treg Plasticity to Th17 via Enhancing Trained Immunity.Cells · 2022Article
- The role of Th17 cells: explanation of relationship between periodontitis and COPD?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Effects of SOCS1-overexpressing dendritic cells on Th17- and Treg-related cytokines in COPD mice.BMC pulmonary medicine · 2022Article
- Quercetin Improves Pulmonary Function and Prevents Emphysema Caused by Exposure to Cigarette Smoke in Male Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Observation of the Effect of Singulair Combined With Ketotifen in the Treatment of Acute Exacerbation of Chronic Obstructive Pulmonary Disease With Airway Hyperresponsiveness and Its Influence on Th17/Treg.Frontiers in surgery · 2022Article
- Chronic Exposure to the Combination of Cigarette Smoke and Morphine Decreases CD4Frontiers in immunology · 2022Article
- Implications of regulatory T cells in non-lymphoid tissue physiology and pathophysiology.Frontiers in immunology · 2022Review
- Bufei Decoction Improves Lung-Qi Deficiency Syndrome of Chronic Obstructive Pulmonary Disease in Rats by Regulating the Balance of Th17/Treg Cells.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Cellular senescence is a key mediator of lung aging and susceptibility to infection.Frontiers in immunology · 2022Review
- Editorial: The importance of Th17/Treg imbalance in asthma and COPD development and progression.Frontiers in immunology · 2022Article
- Mettl14-mediated m6A modification enhances the function of Foxp3Frontiers in immunology · 2022Article
- Chronic Obstructive Pulmonary Disease: Epidemiology, Biomarkers, and Paving the Way to Lung Cancer.Journal of clinical medicine · 2021Review
- Th17/Treg Imbalance in Chronic Obstructive Pulmonary Disease: Clinical and Experimental Evidence.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Th17/Treg imbalance contributes to chronic obstructive pulmonary disease (COPD) development and progression. However, intracellular signaling by suppressor of cytokine signaling (SOCS) 1 and SOCS3 and the proteins signal transducer and activator of transcription (STAT) 3 and STAT5 that orchestrate these imbalances are currently poorly understood. Thus, these proteins were investigated in C57BL/6 mice after exposure to cigarette smoke (CS) for 3 and 6 months. The expression of interleukin was measured by ELISA and the density of positive cells in peribronchovascular areas was quantified by immunohistochemistry. We showed that exposure to CS in the 3rd month first induced decreases in the numbers of STAT5+ and pSTAT5+ cells and the expression levels of TGF-β and IL-10. The increases in the numbers of STAT3+ and pSTAT3+ cells and IL-17 expression occurred later (6th month). These findings corroborate the increases in the number of SOCS1+ cells in both the 3rd and 6th months, with concomitant decreases in SOCS3+ cells at the same time points. Our results demonstrated that beginning with the initiation of COPD development, there was a downregulation of the anti-inflammatory response mediated by SOCS and STAT proteins. These results highlight the importance of intracellular signaling in Th17/Treg imbalance and the identification of possible targets for future therapeutic approaches.
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