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Article: Epigenetic regulation of B cells and its role in autoimmune pathogenesis

TitleEpigenetic regulation of B cells and its role in autoimmune pathogenesis
Authors
KeywordsAutoimmune disease
B cells
Biomarker
Epigenetic regulation
Therapy
Issue Date12-Oct-2022
PublisherSpringer Nature [academic journals on nature.com]
Citation
Cellular & Molecular Immunology, 2022, v. 19, n. 11, p. 1215-1234 How to Cite?
Abstract

B cells play a pivotal role in the pathogenesis of autoimmune diseases. Although previous studies have shown many genetic polymorphisms associated with B-cell activation in patients with various autoimmune disorders, progress in epigenetic research has revealed new mechanisms leading to B-cell hyperactivation. Epigenetic mechanisms, including those involving histone modifications, DNA methylation, and noncoding RNAs, regulate B-cell responses, and their dysregulation can contribute to the pathogenesis of autoimmune diseases. Patients with autoimmune diseases show epigenetic alterations that lead to the initiation and perpetuation of autoimmune inflammation. Moreover, many clinical and animal model studies have shown the promising potential of epigenetic therapies for patients. In this review, we present an up-to-date overview of epigenetic mechanisms with a focus on their roles in regulating functional B-cell subsets. Furthermore, we discuss epigenetic dysregulation in B cells and highlight its contribution to the development of autoimmune diseases. Based on clinical and preclinical evidence, we discuss novel epigenetic biomarkers and therapies for patients with autoimmune disorders.


Persistent Identifierhttp://hdl.handle.net/10722/331730
ISSN
2023 Impact Factor: 21.8
2023 SCImago Journal Rankings: 4.838
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorXiao, F-
dc.contributor.authorRui, K-
dc.contributor.authorShi, XF-
dc.contributor.authorWu, HJ-
dc.contributor.authorCai, XY-
dc.contributor.authorLui, KO-
dc.contributor.authorLu, QJ-
dc.contributor.authorBallestar, E-
dc.contributor.authorTian, J-
dc.contributor.authorZou, HJ-
dc.contributor.authorLu, LW-
dc.date.accessioned2023-09-21T06:58:24Z-
dc.date.available2023-09-21T06:58:24Z-
dc.date.issued2022-10-12-
dc.identifier.citationCellular & Molecular Immunology, 2022, v. 19, n. 11, p. 1215-1234-
dc.identifier.issn1672-7681-
dc.identifier.urihttp://hdl.handle.net/10722/331730-
dc.description.abstract<p> B cells play a pivotal role in the pathogenesis of autoimmune diseases. Although previous studies have shown many genetic polymorphisms associated with B-cell activation in patients with various autoimmune disorders, progress in epigenetic research has revealed new mechanisms leading to B-cell hyperactivation. Epigenetic mechanisms, including those involving histone modifications, DNA methylation, and noncoding RNAs, regulate B-cell responses, and their dysregulation can contribute to the pathogenesis of autoimmune diseases. Patients with autoimmune diseases show epigenetic alterations that lead to the initiation and perpetuation of autoimmune inflammation. Moreover, many clinical and animal model studies have shown the promising potential of epigenetic therapies for patients. In this review, we present an up-to-date overview of epigenetic mechanisms with a focus on their roles in regulating functional B-cell subsets. Furthermore, we discuss epigenetic dysregulation in B cells and highlight its contribution to the development of autoimmune diseases. Based on clinical and preclinical evidence, we discuss novel epigenetic biomarkers and therapies for patients with autoimmune disorders. <br></p>-
dc.languageeng-
dc.publisherSpringer Nature [academic journals on nature.com]-
dc.relation.ispartofCellular & Molecular Immunology-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectAutoimmune disease-
dc.subjectB cells-
dc.subjectBiomarker-
dc.subjectEpigenetic regulation-
dc.subjectTherapy-
dc.titleEpigenetic regulation of B cells and its role in autoimmune pathogenesis-
dc.typeArticle-
dc.identifier.doi10.1038/s41423-022-00933-7-
dc.identifier.scopuseid_2-s2.0-85139659665-
dc.identifier.volume19-
dc.identifier.issue11-
dc.identifier.spage1215-
dc.identifier.epage1234-
dc.identifier.eissn2042-0226-
dc.identifier.isiWOS:000865910200001-
dc.identifier.issnl1672-7681-

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