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High levels of EPSTI1 enhance IFN-β-mediated HLA-A expression and chemokine secretion in myoblasts in dermatomyositis.

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Τίτλος: High levels of EPSTI1 enhance IFN-β-mediated HLA-A expression and chemokine secretion in myoblasts in dermatomyositis.
Συγγραφείς: Li, Xiaojing, Ding, Ting, Xiao, Yizhi, Zhou, Junyu, Huang, Ting, Xie, Shasha, Meng, Qiming, He, Weijia, Zhu, Hongling, Luo, Hui
Πηγή: Rheumatology; Oct2025, Vol. 64 Issue 10, p5529-5538, 10p
Θεματικοί όροι: RNA analysis, Muscle analysis, Chemokines, Dermatomyositis, NF-kappa B, In vitro studies, Small interfering RNA, Carrier proteins, Mononuclear leukocytes, Skeletal muscle, T-test (Statistics), Data analysis, Research funding, Polymerase chain reaction, Enzyme-linked immunosorbent assay, Kruskal-Wallis Test, Cellular signal transduction, Electroporation, Retrospective studies, Mann Whitney U Test, Gene expression, Immunohistochemistry, Genes, Interferons, Messenger RNA, Cell culture, Antigens, Gene expression profiling, Western immunoblotting, Medical records, Acquisition of data, One-way analysis of variance, Statistics, Stem cells, Stains & staining (Microscopy), Data analysis software, HLA-B27 antigen, Immunity, Interleukins, Muscles, Sequence analysis
Περίληψη: Objectives Epithelial-Stromal Interaction 1 (EPSTI1), an IFN-related gene that has emerged as a gene of notable interest, plays a multifaceted role in cellular function and disease processes. However, the precise role of EPSTI1 in the context of DM remains elusive and requires further exploration. Methods To investigate EPSTI1 expression in DM, we analysed two transcriptome datasets, peripheral blood mononuclear cells (PBMCs) and muscle tissues from our DM cohort. We further validated the findings using RT-qPCR and immunohistochemical staining within our idiopathic inflammatory myopathy (IIM) cohort. Through small interfering RNA–mediated knockdown, we delved into the function and underlying mechanisms of EPSTI1 in DM patients. Results EPSTI1 is significantly upregulated in both PBMCs and muscle tissues of DM patients. A notable positive correlation between EPSTI1 expression and IFN-stimulating genes accompanies this upregulation. Furthermore, EPSTI1 levels were markedly elevated in IFN-β-stimulated myoblasts. Functional studies have shown that downregulation of EPSTI1 inhibits multiple immune and inflammatory pathways, including antigen processing and presentation, chemokine-mediated signalling, IFN signalling, IL-1-mediated signalling, nuclear factor (NF)-κB-inducing kinase (NIK)/NF-κB signalling. EPSTI1 was involved in the expression of HLA-A and the secretion of chemokines in myoblasts mediated by IFN-β. Conclusion EPSTI1 might play an essential role in promoting muscle inflammation in DM by regulating the expression of HLA-A and the secretion of chemokines in myoblasts. Targeting EPSTI1 may represent a novel therapeutic approach for reducing muscle inflammation and damage in dermatomyositis (DM) patients. [ABSTRACT FROM AUTHOR]
Copyright of Rheumatology is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Label: Title
  Group: Ti
  Data: High levels of EPSTI1 enhance IFN-β-mediated HLA-A expression and chemokine secretion in myoblasts in dermatomyositis.
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  Data: <searchLink fieldCode="AR" term="%22Li%2C+Xiaojing%22">Li, Xiaojing</searchLink><br /><searchLink fieldCode="AR" term="%22Ding%2C+Ting%22">Ding, Ting</searchLink><br /><searchLink fieldCode="AR" term="%22Xiao%2C+Yizhi%22">Xiao, Yizhi</searchLink><br /><searchLink fieldCode="AR" term="%22Zhou%2C+Junyu%22">Zhou, Junyu</searchLink><br /><searchLink fieldCode="AR" term="%22Huang%2C+Ting%22">Huang, Ting</searchLink><br /><searchLink fieldCode="AR" term="%22Xie%2C+Shasha%22">Xie, Shasha</searchLink><br /><searchLink fieldCode="AR" term="%22Meng%2C+Qiming%22">Meng, Qiming</searchLink><br /><searchLink fieldCode="AR" term="%22He%2C+Weijia%22">He, Weijia</searchLink><br /><searchLink fieldCode="AR" term="%22Zhu%2C+Hongling%22">Zhu, Hongling</searchLink><br /><searchLink fieldCode="AR" term="%22Luo%2C+Hui%22">Luo, Hui</searchLink>
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  Data: Rheumatology; Oct2025, Vol. 64 Issue 10, p5529-5538, 10p
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– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Objectives Epithelial-Stromal Interaction 1 (EPSTI1), an IFN-related gene that has emerged as a gene of notable interest, plays a multifaceted role in cellular function and disease processes. However, the precise role of EPSTI1 in the context of DM remains elusive and requires further exploration. Methods To investigate EPSTI1 expression in DM, we analysed two transcriptome datasets, peripheral blood mononuclear cells (PBMCs) and muscle tissues from our DM cohort. We further validated the findings using RT-qPCR and immunohistochemical staining within our idiopathic inflammatory myopathy (IIM) cohort. Through small interfering RNA–mediated knockdown, we delved into the function and underlying mechanisms of EPSTI1 in DM patients. Results EPSTI1 is significantly upregulated in both PBMCs and muscle tissues of DM patients. A notable positive correlation between EPSTI1 expression and IFN-stimulating genes accompanies this upregulation. Furthermore, EPSTI1 levels were markedly elevated in IFN-β-stimulated myoblasts. Functional studies have shown that downregulation of EPSTI1 inhibits multiple immune and inflammatory pathways, including antigen processing and presentation, chemokine-mediated signalling, IFN signalling, IL-1-mediated signalling, nuclear factor (NF)-κB-inducing kinase (NIK)/NF-κB signalling. EPSTI1 was involved in the expression of HLA-A and the secretion of chemokines in myoblasts mediated by IFN-β. Conclusion EPSTI1 might play an essential role in promoting muscle inflammation in DM by regulating the expression of HLA-A and the secretion of chemokines in myoblasts. Targeting EPSTI1 may represent a novel therapeutic approach for reducing muscle inflammation and damage in dermatomyositis (DM) patients. [ABSTRACT FROM AUTHOR]
– Name: Abstract
  Label:
  Group: Ab
  Data: <i>Copyright of Rheumatology is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1093/rheumatology/keaf297
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        Text: English
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      – TitleFull: High levels of EPSTI1 enhance IFN-β-mediated HLA-A expression and chemokine secretion in myoblasts in dermatomyositis.
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            – D: 01
              M: 10
              Text: Oct2025
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