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The epigenetic face of systemic lupus erythematosus

Author(s): Ballestar E, Esteller M, Richardson BC

Abstract

Systemic lupus erythematosus (SLE) is an archetypical systemic, autoimmune inflammatory disease characterized by the production of autoantibodies to multiple nuclear Ags. Apoptotic defects and impaired removal of apoptotic cells contribute to an overload of autoantigens that become available to initiate an autoimmune response. Besides the well-recognized genetic susceptibility to SLE, epigenetic factors are important in the onset of the disease, as even monozygotic twins are usually discordant for the disease. Changes in DNA methylation and histone modifications, the major epigenetic marks, are a hallmark in genes that undergo epigenetic deregulation in disease. In SLE, global and gene-specific DNA methylation changes have been demonstrated to occur. Moreover, histone deacetylase inhibitors reverse the skewed expression of multiple genes involved in SLE. In the present study, we discuss the implications of epigenetic alterations in the development and progression of SLE and how epigenetic drugs constitute a promising source of therapy to treat this disease.

Although the existence of a genetic determinant of many diseases is well established, it is generally accepted that environmental factors, including diet and lifestyle, modulate the susceptibility, in part, through epigenetic changes (1). However, although many studies have corroborated these ideas and led to the identification of the genetic defects involved in many diseases, virtually no epigenetic information has been routinely or systematically collected at the genome level. In recent years, we have witnessed an increasing interest in the role of epigenetic modifications in the etiology of human disease.

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