{"title":"Methyl-CpG-Binding Domain Protein 2 is Involved in Th17 Cell Differentiation by Negatively Regulating Leptin Expression.","authors":"Yang Xia, Xiufeng Zhang, Dingjiang Wu","doi":"10.2174/0115665240341834250121080510","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Among Th lineages from naïve CD4+T cells, Th17 cells producing IL-17 are strongly related to the pathogenesis of neutrophilic asthma. Leptin is involved in inflammation and immunity. Little is known about MBD2's epigenetic regulation in CD4+T cell differentiation.</p><p><strong>Objective: </strong>Our study is intended to delve into the mode by which MBD2 interacts with Leptin to govern Th17 cell differentiation.</p><p><strong>Methods: </strong>CD4+T cells were harvested from the spleen tissue of C57BL/6 mice. Th17 cell differentiation was determined by flow cytometry, and ELISA measured IL-17. Western blot and RT-qPCR were employed to detect the expression of MBD2, Leptin and RORγt. CO-IP was utilized to assess the relationship between MBD2 and Leptin.</p><p><strong>Results: </strong>Under the overexpression or silencing of the MBD2 and Leptin genes, the differentiation of Th17 cells, IL-17 secretion, and RORγt expression all manifested positive changes. Leptin expression showed a positive variance upon overexpression or silencing of the MBD2 gene; however, there was no significant disparity in the expression of MBD2 under the overexpression or silencing of the Leptin gene. MBD2 can interact directly with Leptin.</p><p><strong>Conclusion: </strong>MBD2 is capable of inducing the differentiation of naïve CD4+T cells into Th17 cells by augmenting the expression of Leptin.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.2000,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current molecular medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2174/0115665240341834250121080510","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Among Th lineages from naïve CD4+T cells, Th17 cells producing IL-17 are strongly related to the pathogenesis of neutrophilic asthma. Leptin is involved in inflammation and immunity. Little is known about MBD2's epigenetic regulation in CD4+T cell differentiation.
Objective: Our study is intended to delve into the mode by which MBD2 interacts with Leptin to govern Th17 cell differentiation.
Methods: CD4+T cells were harvested from the spleen tissue of C57BL/6 mice. Th17 cell differentiation was determined by flow cytometry, and ELISA measured IL-17. Western blot and RT-qPCR were employed to detect the expression of MBD2, Leptin and RORγt. CO-IP was utilized to assess the relationship between MBD2 and Leptin.
Results: Under the overexpression or silencing of the MBD2 and Leptin genes, the differentiation of Th17 cells, IL-17 secretion, and RORγt expression all manifested positive changes. Leptin expression showed a positive variance upon overexpression or silencing of the MBD2 gene; however, there was no significant disparity in the expression of MBD2 under the overexpression or silencing of the Leptin gene. MBD2 can interact directly with Leptin.
Conclusion: MBD2 is capable of inducing the differentiation of naïve CD4+T cells into Th17 cells by augmenting the expression of Leptin.
期刊介绍:
Current Molecular Medicine is an interdisciplinary journal focused on providing the readership with current and comprehensive reviews/ mini-reviews, original research articles, short communications/letters and drug clinical trial studies on fundamental molecular mechanisms of disease pathogenesis, the development of molecular-diagnosis and/or novel approaches to rational treatment. The reviews should be of significant interest to basic researchers and clinical investigators in molecular medicine. Periodically the journal invites guest editors to devote an issue on a basic research area that shows promise to advance our understanding of the molecular mechanism(s) of a disease or has potential for clinical applications.