The functions of CD4 T-helper lymphocytes in chronic obstructive pulmonary disease

Qin, Keru; Xu, Baixue; Pang, Min; Wang, Hailong; Yu, Bin

doi:10.3724/abbs.2021009

Cited by 16 publications

(16 citation statements)

References 57 publications

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“…Both asthma and COPD involve chronic airway in ammation, but they have different underlying mechanisms. In asthma, there is typically eosinophilic in ammation driven by a Th2 immune response 65 , while COPD is characterized by neutrophilic in ammation associated with Th1 and Th17-driven in ammation 10,66,67 . In both conditions, macrophages play a central role in the recruitment and activation of neutrophils and eosinophils [11][12][13]68 .…”

Section: Discussionmentioning

confidence: 99%

“…In asthma, in ammation is primarily driven by Th2 cell-mediated responses, leading to eosinophilic in ammation and an increase in cytokines like IL-4, IL-5, and IL-13 9 . On the other hand, COPD is characterized by in ammation with a higher presence of neutrophils and a dominance of Th1 and Th17 cell-mediated responses 10 . In both conditions, macrophages, the primary immune cells in the lungs, play crucial roles in the immune response, defense against infections, tissue homeostasis, and in ammation resolution 11 .…”

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confidence: 99%

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PPARγ Attenuates Cellular Senescence of Alveolar Macrophages in Asthma- COPD Overlap

Wan,

Srika,

Xie

et al. 2024

Preprint

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Asthma-chronic obstructive pulmonary disease (COPD) overlap (ACO) represents a complex condition characterized by shared clinical and pathophysiological features of asthma and COPD in older individuals. However, the pathophysiology of ACO remains unexplored. We aimed to identify the major inflammatory cells in ACO, examine senescence within these cells, and elucidate the genes responsible for regulating senescence. Bioinformatic analyses were performed to investigate major cell types and cellular senescence signatures in a public single-cell RNA sequencing (scRNA-Seq) dataset derived from the lung tissues of patients with ACO. Similar analyses were carried out in an independent cohort study Immune Mechanisms Severe Asthma (IMSA), which included bulk RNA-Seq and CyTOF data from bronchoalveolar lavage fluid (BALF) samples. The analysis of the scRNA-Seq data revealed that monocytes/ macrophages were the predominant cell type in the lung tissues of ACO patients, constituting more than 50% of the cells analyzed. Lung monocytes/macrophages from patients with ACO exhibited a lower prevalence of senescence as defined by lower enrichment scores of SenMayo and expression levels of cellular senescence markers. Intriguingly, analysis of the IMSA dataset showed similar results in patients with severe asthma. They also exhibited a lower prevalence of senescence, particularly in airway CD206 + macrophages, along with increased cytokine expression (e.g., IL-4, IL-13, and IL-22). Further exploration identified alveolar macrophages as a major subtype of monocytes/macrophages driving cellular senescence in ACO. Differentially expressed genes related to oxidation-reduction, cytokines, and growth factors were implicated in regulating senescence in alveolar macrophages. PPARγ (Peroxisome Proliferator-Activated Receptor Gamma) emerged as one of the predominant regulators modulating the senescent signature of alveolar macrophages in ACO. Collectively, the findings suggest that senescence in macrophages, particularly alveolar macrophages, plays a crucial role in the pathophysiology of ACO. Furthermore, PPARγ may represent a potential therapeutic target for interventions aimed at modulating senescence-associated processes in ACO.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

PPARγ Attenuates Cellular Senescence of Alveolar Macrophages in Asthma- COPD Overlap

Wan,

Srika,

Xie

et al. 2024

Preprint

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“…For example, Th1 and Th17 T lymphocytes play an important role in the inflammatory process of COPD or non-type2 asthma. 23,24 A combined analysis of genome-wide association studies (GWAS) from large COPD case-control studies (i.e., COPDGene, GenKOLS, and ECLIPSE) identified several genes associated with CD4 T cell response. 25 GWAS of lung function identified that the Th1 pathway genes modify lung function in asthmatic subjects.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary comorbidities in psoriasis are associated with a high risk of respiratory failure

et al. 2023

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Objectives To identify respiratory comorbidities associated with a high risk of developing respiratory failure in subjects with psoriasis. Methods This was a cross-sectional analysis of data from subjects enrolled in the UK Biobank cohort. All diagnoses were self-reported. The risk of each respiratory comorbidity was compared by logistic regression models adjusting for age, sex, weight, diabetes mellitus, and smoking history; the risk of comorbid respiratory failure for each pulmonary comorbidity was also compared. Results Of the 472,782 Caucasian subjects in the database, 3,285 self-reported a diagnosis of psoriasis. More men and smokers reported psoriasis and were older, had higher weight and body mass index, and lower pulmonary function than non-psoriatic subjects. Those with psoriasis were at significantly higher risk for multiple pulmonary comorbidities compared to those without psoriasis. Furthermore, those with psoriasis had a higher risk for respiratory failure accompanied by asthma and airflow limitation than non-psoriatic subjects. Conclusions Subjects with psoriasis and pulmonary comorbidities, such as asthma and airflow limitation, are at increased risk for respiratory failure. Common immunopathological links implicating a ‘skin-lung axis’ may underlie psoriasis and pulmonary comorbidities.

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“…Programmed cell death in COPD has been characterised as another feature of COPD development, which is triggered by cigarette smoke, often followed by persistent inflammation, owing to the release of damageassociated molecular patterns (DAMPs) [28]. KEGG analysis showed enrichment in Th1, Th2, and Th17 cell differentiation, the proportions of which were reported to increase in patients with COPD [29]. Moreover, another study also showed that different inflammatory phenotypes may be related to different bacterial species in the airways of patients with COPD [30].…”

Section: Discussionmentioning

confidence: 99%

Combining single-cell RNA sequencing of peripheral blood mononuclear cells and exosomal transcriptome to reveal the cellular and genetic profiles in COPD

et al. 2022

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Background It has been a long-held consensus that immune reactions primarily mediate the pathology of chronic obstructive pulmonary disease (COPD), and that exosomes may participate in immune regulation in COPD. However, the relationship between exosomes and peripheral immune status in patients with COPD remains unclear. Methods In this study, we sequenced plasma exosomes and performed single-cell RNA sequencing on peripheral blood mononuclear cells (PBMCs) from patients with COPD and healthy controls. Finally, we constructed competing endogenous RNA (ceRNA) and protein–protein interaction (PPI) networks to delineate the interactions between PBMCs and exosomes within COPD. Results We identified 135 mRNAs, 132 lncRNAs, and 359 circRNAs from exosomes that were differentially expressed in six patients with COPD compared with four healthy controls. Functional enrichment analyses revealed that many of these differentially expressed RNAs were involved in immune responses including defending viral infection and cytokine–cytokine receptor interaction. We also identified 18 distinct cell clusters of PBMCs in one patient and one control by using an unsupervised cluster analysis called uniform manifold approximation and projection (UMAP). According to resultant cell identification, it was likely that the proportions of monocytes, dendritic cells, and natural killer cells increased in the COPD patient we tested, meanwhile the proportions of B cells, CD4 + T cells, and naïve CD8 + T cells declined. Notably, CD8 + T effector memory CD45RA + (Temra) cell and CD8 + effector memory T (Tem) cell levels were elevated in patient with COPD, which were marked by their lower capacity to differentiate due to their terminal differentiation state and lower reactive capacity to viral pathogens. Conclusions We generated exosomal RNA profiling and single-cell transcriptomic profiling of PBMCs in COPD, described possible connection between impaired immune function and COPD development, and finally determined the possible role of exosomes in mediating local and systemic immune reactions.

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The functions of CD4 T-helper lymphocytes in chronic obstructive pulmonary disease

Cited by 16 publications

References 57 publications

PPARγ Attenuates Cellular Senescence of Alveolar Macrophages in Asthma- COPD Overlap

PPARγ Attenuates Cellular Senescence of Alveolar Macrophages in Asthma- COPD Overlap

Pulmonary comorbidities in psoriasis are associated with a high risk of respiratory failure

Combining single-cell RNA sequencing of peripheral blood mononuclear cells and exosomal transcriptome to reveal the cellular and genetic profiles in COPD

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