{"title":"B细胞记忆形成的表观遗传调控:B细胞表观遗传重编程的平衡模型。","authors":"Carlos Valverde-Hernandez","doi":"10.1155/jimr/9328523","DOIUrl":null,"url":null,"abstract":"<p><p>The formation of B cell immunological memory happens after the first encounter with a pathogen. At the germinal center (GC), B cells experience complex transcriptional and epigenetic transitions to differentiate into memory B cells (MBCs) and plasma cells (PCs). In particular, the differentiation of GC B cells into MBCs has been poorly understood, and no clear conclusions on the signals and transcription factors leading to this cell fate have been identified. Recent discoveries in epigenetics and immune memory have elucidated the essential role of epigenetic regulators in establishing the memory B cell (MBC) fate. DNA methylation regulators, histone modifiers, noncoding RNAs (ncRNAs), and chromatin remodelers orchestrate a dynamic reprograming of the MBC phenotype. Positive and negative epigenetic regulators of the B cell program collaborate at each differentiation stage and allow for complex chromatin topology rearrangements and dynamic exposure to transcription and translation. Following MBC fate determination at the GC, the acquired epigenetic modifications induce a poised regulatory state where genes are epigenetically marked to remain transcriptionally inactive, but primed for rapid activation upon stimuli. Thus, a poised epigenetic control over gene expression governs MBC formation and a novel model of epigenetic reprograming is proposed. This model provides a novel perspective on how the B cell fate is determined in the GC and memory is formed, offering insights for improved vaccination and therapeutical approaches.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2025 ","pages":"9328523"},"PeriodicalIF":3.6000,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12289371/pdf/","citationCount":"0","resultStr":"{\"title\":\"Epigenetic Regulation of B Cell Memory Formation: A Poised Model for B Cell Epigenetic Reprograming.\",\"authors\":\"Carlos Valverde-Hernandez\",\"doi\":\"10.1155/jimr/9328523\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The formation of B cell immunological memory happens after the first encounter with a pathogen. At the germinal center (GC), B cells experience complex transcriptional and epigenetic transitions to differentiate into memory B cells (MBCs) and plasma cells (PCs). In particular, the differentiation of GC B cells into MBCs has been poorly understood, and no clear conclusions on the signals and transcription factors leading to this cell fate have been identified. Recent discoveries in epigenetics and immune memory have elucidated the essential role of epigenetic regulators in establishing the memory B cell (MBC) fate. DNA methylation regulators, histone modifiers, noncoding RNAs (ncRNAs), and chromatin remodelers orchestrate a dynamic reprograming of the MBC phenotype. Positive and negative epigenetic regulators of the B cell program collaborate at each differentiation stage and allow for complex chromatin topology rearrangements and dynamic exposure to transcription and translation. Following MBC fate determination at the GC, the acquired epigenetic modifications induce a poised regulatory state where genes are epigenetically marked to remain transcriptionally inactive, but primed for rapid activation upon stimuli. Thus, a poised epigenetic control over gene expression governs MBC formation and a novel model of epigenetic reprograming is proposed. This model provides a novel perspective on how the B cell fate is determined in the GC and memory is formed, offering insights for improved vaccination and therapeutical approaches.</p>\",\"PeriodicalId\":15952,\"journal\":{\"name\":\"Journal of Immunology Research\",\"volume\":\"2025 \",\"pages\":\"9328523\"},\"PeriodicalIF\":3.6000,\"publicationDate\":\"2025-07-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12289371/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Immunology Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1155/jimr/9328523\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Immunology Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1155/jimr/9328523","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
Epigenetic Regulation of B Cell Memory Formation: A Poised Model for B Cell Epigenetic Reprograming.
The formation of B cell immunological memory happens after the first encounter with a pathogen. At the germinal center (GC), B cells experience complex transcriptional and epigenetic transitions to differentiate into memory B cells (MBCs) and plasma cells (PCs). In particular, the differentiation of GC B cells into MBCs has been poorly understood, and no clear conclusions on the signals and transcription factors leading to this cell fate have been identified. Recent discoveries in epigenetics and immune memory have elucidated the essential role of epigenetic regulators in establishing the memory B cell (MBC) fate. DNA methylation regulators, histone modifiers, noncoding RNAs (ncRNAs), and chromatin remodelers orchestrate a dynamic reprograming of the MBC phenotype. Positive and negative epigenetic regulators of the B cell program collaborate at each differentiation stage and allow for complex chromatin topology rearrangements and dynamic exposure to transcription and translation. Following MBC fate determination at the GC, the acquired epigenetic modifications induce a poised regulatory state where genes are epigenetically marked to remain transcriptionally inactive, but primed for rapid activation upon stimuli. Thus, a poised epigenetic control over gene expression governs MBC formation and a novel model of epigenetic reprograming is proposed. This model provides a novel perspective on how the B cell fate is determined in the GC and memory is formed, offering insights for improved vaccination and therapeutical approaches.
期刊介绍:
Journal of Immunology Research is a peer-reviewed, Open Access journal that provides a platform for scientists and clinicians working in different areas of immunology and therapy. The journal publishes research articles, review articles, as well as clinical studies related to classical immunology, molecular immunology, clinical immunology, cancer immunology, transplantation immunology, immune pathology, immunodeficiency, autoimmune diseases, immune disorders, and immunotherapy.