Abstract
The imbalance between pro- and anti-inflammatory immune responses mediated by Th17 and Treg cells is deeply involved in the development and progression of inflammation in chronic obstructive pulmonary disease (COPD). Several clinical and experimental studies have described the Th17/Treg imbalance in COPD progression. Due to its importance, many studies have also evaluated the effect of different treatments targeting Th17/Treg cells. However, discrepant results have been observed among different lung compartments, different COPD stages or local and systemic markers. Thus, the data must be carefully examined. In this context, this review explores and summarizes the recent outcomes of Th17/Treg imbalance in COPD development and progression in clinical, experimental and in vitro studies.
Highlights
Chronic obstructive pulmonary disease (COPD) is an inflammatory disease characterized by airway and/or alveolar abnormalities that lead to persistent airflow limitations and respiratory symptoms (1)
COPD patients, especially when they have the disease in severe stages and during exacerbations, present systemic inflammation, which is associated with an accelerated decrease in lung function
They demonstrated a progressive increase in both Th17 and Treg cell subsets in peripheral blood mononuclear cells (PBMCs) from COPD patients and smokers without COPD compared to healthy subjects (59)
Summary
Chronic obstructive pulmonary disease (COPD) is an inflammatory disease characterized by airway and/or alveolar abnormalities that lead to persistent airflow limitations and respiratory symptoms (1). COPD patients, especially when they have the disease in severe stages and during exacerbations, present systemic inflammation, which is associated with an accelerated decrease in lung function This inflammation is characterized by increased circulating proinflammatory cytokines and chemokines, the levels of acute phase proteins, and abnormalities in circulating cells (4). CD8+ T cells are the subtype of lymphocytes present in increased amounts in patients with COPD and they release proteolytic enzymes such as perforins and granzyme-B These enzymes cause the death of structural cells by apoptosis or necrosis leading to the degradation of the extracellular matrix and remodelling, which results in the. These discrepancies are observed when analyses are performed in different lung compartments or when comparing samples from lungs to peripheral blood In this context, this review intends to explore and summarize the recent outcomes of Th17/Treg imbalance in COPD development and progression in clinical, experimental and in vitro studies
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
