title: Epigenetic Control of B Cell Development and B-Cell-Related Immune Disorders.
abstract: B lymphocytes are generally recognized as the essential component of humoral immunity and also a regulator of innate immunity. The development of B cells is precisely regulated by a variety of factors via different mechanisms, including cytokine/cytokine receptors, signal transduction molecules, and transcription factors. Recent findings suggest that epigenetic factors, such as DNA methylation, histone modification, and non-coding RNA, play critical roles in establishing B cell lineage-specific gene expression profiles to define and sustain B cell identity and function. Epigenetic modifications are also sensitive to external stimuli and might bridge genetic and environmental factors in the pathogenesis or control of B-cell-related immune disorders, such as autoimmune diseases, lymphoma, and leukemia. Better understanding of the epigenetic mechanisms for regulating B cell development and involving B cell abnormal differentiation and function will shed light on the design of new therapeutic approaches to B-cell-related diseases, and potential candidates of epigenetic modulators may be identified to target epigenetic pathways to prevent or treat B cell disorders. We summarize the relevance of epigenetic marks and landscapes in the stages of B cell development, discuss the interaction of the transcriptional networks and epigenetic changes, and review the involvement of epigenetic risk in the pathogenesis of B-cell-related diseases. Understanding how specific epigenetic alterations contribute to the development of B-cell-related autoimmunity and malignancies is instrumental to control B cell disorders.
authors.affiliation: Center for Translational Medicine, Changzheng Hospital, Second Military Medical University, Shanghai, China. baoy_smmu@163.com.|National Key Laboratory of Molecular Medical Biology & Department of Immunology, Chinese Academy of Medical Sciences, Beijing, China. baoy_smmu@163.com.
authors.forename: Yan
authors.initials: Y
authors.lastname: Bao
authors.affiliation: National Key Laboratory of Molecular Medical Biology & Department of Immunology, Chinese Academy of Medical Sciences, Beijing, China. caoxt@immunol.org.
authors.forename: Xuetao
authors.initials: X
authors.lastname: Cao
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology / Q000378:metabolism; D001402:B-Lymphocytes / Q000166:cytology* / Q000502:physiology*; D002454:Cell Differentiation; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000378:metabolism; D044127:Epigenesis, Genetic; D005786:Gene Expression Regulation; D006801:Humans; D007154:Immune System Diseases / Q000209:etiology* / Q000378:metabolism*; D015448:Leukemia, B-Cell / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D008213:Lymphocyte Activation / Q000235:genetics / Q000276:immunology; D016393:Lymphoma, B-Cell / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D038041:Lymphopoiesis / Q000235:genetics; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D014157:Transcription Factors
keywords: Autoimmune disease; B cell; B cell malignancies; Development; Differentiation; Epigenetic regulation