{"title":"MBD2在免疫细胞发育、功能和自身免疫性疾病中的作用。","authors":"Yunfei Zhang, Yufeng Fan, Ying Hu, Xiaocui Wang, Bin Wen, Xuemei Duan, Haonan Li, Shumin Dong, Ze Yan, Weiwei Zhang, Yukai Jing","doi":"10.1038/s41420-025-02563-0","DOIUrl":null,"url":null,"abstract":"<p><p>DNA methylation is a key epigenetic modification that regulates gene expression, cell differentiation, and genome stability. Aberrant DNA methylation patterns, including the hypermethylation or global hypomethylation of tumor suppressor genes, are strongly associated with various human diseases, such as cancer, autoimmune disorders, and metabolic syndrome. DNA methylation predominantly occurs at CpG dinucleotides, influencing transcription by altering chromatin structure and accessibility. MBD2 (Methyl-CpG-binding proteins 2) play a crucial role in interpreting these epigenetic marks and regulating downstream gene expression. In disease contexts, aberrant DNA methylation disrupts cellular homeostasis by silencing key regulatory genes or activating pathological pathways. Current research primarily focuses on MBD2 in cancer, with less emphasis on its role in autoimmune diseases. This review discusses the role of MBD2 in regulating immune cell development and differentiation through epigenetic mechanisms, particularly DNA methylation and its regulatory components. Furthermore, it highlights the mechanistic contributions of MBD2 to autoimmune diseases such as systemic lupus erythematosus and evaluates its potential as a novel therapeutic target for these conditions.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"280"},"PeriodicalIF":7.0000,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12177077/pdf/","citationCount":"0","resultStr":"{\"title\":\"The role of MBD2 in immune cell development, function, and autoimmune diseases.\",\"authors\":\"Yunfei Zhang, Yufeng Fan, Ying Hu, Xiaocui Wang, Bin Wen, Xuemei Duan, Haonan Li, Shumin Dong, Ze Yan, Weiwei Zhang, Yukai Jing\",\"doi\":\"10.1038/s41420-025-02563-0\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>DNA methylation is a key epigenetic modification that regulates gene expression, cell differentiation, and genome stability. Aberrant DNA methylation patterns, including the hypermethylation or global hypomethylation of tumor suppressor genes, are strongly associated with various human diseases, such as cancer, autoimmune disorders, and metabolic syndrome. DNA methylation predominantly occurs at CpG dinucleotides, influencing transcription by altering chromatin structure and accessibility. MBD2 (Methyl-CpG-binding proteins 2) play a crucial role in interpreting these epigenetic marks and regulating downstream gene expression. In disease contexts, aberrant DNA methylation disrupts cellular homeostasis by silencing key regulatory genes or activating pathological pathways. Current research primarily focuses on MBD2 in cancer, with less emphasis on its role in autoimmune diseases. This review discusses the role of MBD2 in regulating immune cell development and differentiation through epigenetic mechanisms, particularly DNA methylation and its regulatory components. Furthermore, it highlights the mechanistic contributions of MBD2 to autoimmune diseases such as systemic lupus erythematosus and evaluates its potential as a novel therapeutic target for these conditions.</p>\",\"PeriodicalId\":9735,\"journal\":{\"name\":\"Cell Death Discovery\",\"volume\":\"11 1\",\"pages\":\"280\"},\"PeriodicalIF\":7.0000,\"publicationDate\":\"2025-06-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12177077/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cell Death Discovery\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1038/s41420-025-02563-0\",\"RegionNum\":2,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Death Discovery","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41420-025-02563-0","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
The role of MBD2 in immune cell development, function, and autoimmune diseases.
DNA methylation is a key epigenetic modification that regulates gene expression, cell differentiation, and genome stability. Aberrant DNA methylation patterns, including the hypermethylation or global hypomethylation of tumor suppressor genes, are strongly associated with various human diseases, such as cancer, autoimmune disorders, and metabolic syndrome. DNA methylation predominantly occurs at CpG dinucleotides, influencing transcription by altering chromatin structure and accessibility. MBD2 (Methyl-CpG-binding proteins 2) play a crucial role in interpreting these epigenetic marks and regulating downstream gene expression. In disease contexts, aberrant DNA methylation disrupts cellular homeostasis by silencing key regulatory genes or activating pathological pathways. Current research primarily focuses on MBD2 in cancer, with less emphasis on its role in autoimmune diseases. This review discusses the role of MBD2 in regulating immune cell development and differentiation through epigenetic mechanisms, particularly DNA methylation and its regulatory components. Furthermore, it highlights the mechanistic contributions of MBD2 to autoimmune diseases such as systemic lupus erythematosus and evaluates its potential as a novel therapeutic target for these conditions.
期刊介绍：
Cell Death Discovery is a multidisciplinary, international, online-only, open access journal, dedicated to publishing research at the intersection of medicine with biochemistry, pharmacology, immunology, cell biology and cell death, provided it is scientifically sound. The unrestricted access to research findings in Cell Death Discovery will foster a dynamic and highly productive dialogue between basic scientists and clinicians, as well as researchers in industry with a focus on cancer, neurobiology and inflammation research. As an official journal of the Cell Death Differentiation Association (ADMC), Cell Death Discovery will build upon the success of Cell Death & Differentiation and Cell Death & Disease in publishing important peer-reviewed original research, timely reviews and editorial commentary.
Cell Death Discovery is committed to increasing the reproducibility of research. To this end, in conjunction with its sister journals Cell Death & Differentiation and Cell Death & Disease, Cell Death Discovery provides a unique forum for scientists as well as clinicians and members of the pharmaceutical and biotechnical industry. It is committed to the rapid publication of high quality original papers that relate to these subjects, together with topical, usually solicited, reviews, editorial correspondence and occasional commentaries on controversial and scientifically informative issues.
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