Deleterious Role of Th9 Cells in Pulmonary Fibrosis

Deng, Kui Miao; Yang, Xiang; Luo, Qun; She, Yi Xin; Yu, Qing; Tang, Xiao Xiao

doi:10.3390/cells10113209

Cited by 16 publications

(10 citation statements)

References 59 publications

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“…Increasing evidences indicate that immune cells are linked to the development of IPF ( 1 , 19 , 41 , 42 ). Kreuter et al.…”

Section: Discussionmentioning

confidence: 99%

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Identification and validation of autophagy-related gene expression for predicting prognosis in patients with idiopathic pulmonary fibrosis

Huang

Xu²,

Chen³

et al. 2022

Front. Immunol.

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BackgroundIdiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and fatal fibrotic pulmonary disease with unknow etiology. Owing to lack of reliable prognostic biomarkers and effective treatment measures, patients with IPF usually exhibit poor prognosis. The aim of this study is to establish a risk score prognostic model for predicting the prognosis of patients with IPF based on autophagy-related genes.MethodsThe GSE70866 dataset was obtained from the gene expression omnibus (GEO) database. The autophagy-related genes were collected from the Molecular Signatures Database (MSigDB). Gene enrichment analysis for differentially expressed genes (DEGs) was performed to explore the function of DEGs. Univariate, least absolute shrinkage and selection operator (LASSO), as well as multivariate Cox regression analyses were conducted to identify a multi-gene prognostic model. Receiver operating characteristic (ROC) curve was applied to assess the prediction accuracy of the model. The expression of genes screened from the prognostic model was validated in clinical samples and human lung fibroblasts by qPCR and western blot assays.ResultsAmong the 514 autophagy-related genes, a total of 165 genes were identified as DEGs. These DEGs were enriched in autophagy-related processes and pathways. Based on the univariate, LASSO, and multivariate Cox regression analyses, two genes (MET and SH3BP4) were included for establishing the risk score prognostic model. According to the median value of the risk score, patients with IPF were stratified into high-risk and low-risk groups. Patients in high-risk group had shorter overall survival (OS) than low-risk group in both training and test cohorts. Multivariate regression analysis indicated that prognostic model can act as an independent prognostic indicator for IPF. ROC curve analysis confirmed the reliable predictive value of prognostic model. In the validation experiments, upregulated MET expression and downregulated SH3BP4 expression were observed in IPF lung tissues and TGF-β1-activated human lung fibroblasts, which is consistent with results from microarray data analysis.ConclusionThese findings indicated that the risk score prognostic model based on two autophagy-related genes can effectively predict the prognosis of patients with IPF.

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“…Increasing evidences indicate that immune cells are linked to the development of IPF ( 1 , 19 , 41 , 42 ). Kreuter et al.…”

Section: Discussionmentioning

confidence: 99%

“…Increasing evidences indicate that immune cells are linked to the development of IPF (1,19,41,42). Kreuter et al reported that increased monocyte count was related to elevated risks of IPF progression, hospitalization and mortality for patients with IPF (43).…”

Section: A B Cmentioning

confidence: 99%

Identification and validation of autophagy-related gene expression for predicting prognosis in patients with idiopathic pulmonary fibrosis

Huang

Xu²,

Chen³

et al. 2022

Front. Immunol.

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“…Patients with perivascular fibrosis due to Schistosoma mansoni infection have shown elevated serum IL-9 levels. IPF fibrosis patients as well as a rat model of silica-induced lung fibrosis were both revealed to have considerably increased IL-9 levels [ 115 ]. IL-9 is also markedly elevated in liver cirrhosis patients and is crucial to the development of hepatic fibrosis.…”

Section: Immunity and Fibrosismentioning

confidence: 99%

Fibrosis: Types, Effects, Markers, Mechanisms for Disease Progression, and Its Relation with Oxidative Stress, Immunity, and Inflammation

Antar

Ashour

Marawan

et al. 2023

IJMS

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Most chronic inflammatory illnesses include fibrosis as a pathogenic characteristic. Extracellular matrix (ECM) components build up in excess to cause fibrosis or scarring. The fibrotic process finally results in organ malfunction and death if it is severely progressive. Fibrosis affects nearly all tissues of the body. The fibrosis process is associated with chronic inflammation, metabolic homeostasis, and transforming growth factor-β1 (TGF-β1) signaling, where the balance between the oxidant and antioxidant systems appears to be a key modulator in managing these processes. Virtually every organ system, including the lungs, heart, kidney, and liver, can be affected by fibrosis, which is characterized as an excessive accumulation of connective tissue components. Organ malfunction is frequently caused by fibrotic tissue remodeling, which is also frequently linked to high morbidity and mortality. Up to 45% of all fatalities in the industrialized world are caused by fibrosis, which can damage any organ. Long believed to be persistently progressing and irreversible, fibrosis has now been revealed to be a very dynamic process by preclinical models and clinical studies in a variety of organ systems. The pathways from tissue damage to inflammation, fibrosis, and/or malfunction are the main topics of this review. Furthermore, the fibrosis of different organs with their effects was discussed. Finally, we highlight many of the principal mechanisms of fibrosis. These pathways could be considered as promising targets for the development of potential therapies for a variety of important human diseases.

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“…A key cytokine secreted by Th9 cells is IL-9, which has both antifibrotic and profibrotic effects [ 175 ]. However, recent studies have shown that Th9 cells do contribute to pulmonary fibrosis by increasing IL-4-mediated Th2 cell differentiation, and IL-9 neutralisation effectively reduces the degree of pulmonary fibrosis [ 176 ]. Regulatory T cells can also have both anti- [ 177 ] and profibrotic effects [ 178 , 179 ].…”

Section: Immunologic Regulation Of Pulmonary Fibrosismentioning

confidence: 99%

Role of Mesenchymal Stem Cells and Extracellular Vesicles in Idiopathic Pulmonary Fibrosis

Kletukhina

Mutallapova

Titova

et al. 2022

IJMS

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Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial fibrotic disease that leads to disability and death within 5 years of diagnosis. Pulmonary fibrosis is a disease with a multifactorial etiology. The concept of aberrant regeneration of the pulmonary epithelium reveals the pathogenesis of IPF, according to which repeated damage and death of alveolar epithelial cells is the main mechanism leading to the development of progressive IPF. Cell death provokes the migration, proliferation and activation of fibroblasts, which overproduce extracellular matrix, resulting in fibrotic deformity of the lung tissue. Mesenchymal stem cells (MSCs) and extracellular vesicles (EVs) are promising therapies for pulmonary fibrosis. MSCs, and EVs derived from MSCs, modulate the activity of immune cells, inhibit the expression of profibrotic genes, reduce collagen deposition and promote the repair of damaged lung tissue. This review considers the molecular mechanisms of the development of IPF and the multifaceted role of MSCs in the therapy of IPF. Currently, EVs-MSCs are regarded as a promising cell-free therapy tool, so in this review we discuss the results available to date of the use of EVs-MSCs for lung tissue repair.

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Deleterious Role of Th9 Cells in Pulmonary Fibrosis

Cited by 16 publications

References 59 publications

Identification and validation of autophagy-related gene expression for predicting prognosis in patients with idiopathic pulmonary fibrosis

Identification and validation of autophagy-related gene expression for predicting prognosis in patients with idiopathic pulmonary fibrosis

Fibrosis: Types, Effects, Markers, Mechanisms for Disease Progression, and Its Relation with Oxidative Stress, Immunity, and Inflammation

Role of Mesenchymal Stem Cells and Extracellular Vesicles in Idiopathic Pulmonary Fibrosis

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