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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 711))

Abstract

Although not exclusive, mounting evidence supports the fact that DNA methylation at CpG dinucleotides controls B-cell development and the progressive elimination or inactivation of autoreactive B cell. Indeed, the expression of different B cell specific factors, including Pax5, rearrangement of the B-cell receptor (BCR) and cytokine production are tightly controlled by DNA methylation. Among normal B cells, the autoreactive CD5+ B cell sub-population presents a reduced capacity to methylate its DNA that leads to the expression of normally repressed genes, such as the human endogenous retrovirus (HERV). In systemic lupus erythematosus (SLE) patients, the archetype of autoimmune disease, autoreactive B cells are characterized by their inability to induce DNA methylation that prolongs their survival. Finally, treating B cells with demethylating drugs increased their autoreactivity. Altogether this suggests that a deeper comprehension of DNA methylation in B cells may offer opportunities to develop new the rapeutics to control autoreactive B cells.

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© 2011 Landes Bioscience and Springer Science+Business Media

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Garaud, S., Youinou, P., Renaudineau, Y. (2011). DNA Methylation and B-Cell Autoreactivity. In: Ballestar, E. (eds) Epigenetic Contributions in Autoimmune Disease. Advances in Experimental Medicine and Biology, vol 711. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-8216-2_5

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