The epigenetic landscape of B lymphocyte tolerance to self

Abstract

Despite frequent exposures to a variety of potential triggers, including antigens produced by pathogens or commensal microbiota, B-lymphocytes are able to mount highly protective responses to a variety of threats, while remaining tolerant to self-components. A number of cytokines, signaling pathways and transcription factors have been characterized to elucidate the mechanisms underlying B cell tolerance to self. It is, however, unclear how the signals received by B-lymphocytes are converted into complex and sustained patterns of gene expression that can allow production of protective antibodies and maintain immune tolerance to self-components. Mounting evidence now suggests an important role for epigenetic mechanisms in modulating and transmitting signals for B lymphocyte tolerization to self-antigens. It is likely that a better insight into epigenetic regulation of B cell tolerance will lead to development of gene-specific therapeutic approaches that optimize host defense mechanisms to exogenous threats, while preventing development and/or progression of autoimmune inflammatory diseases.