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DNA methylation in systemic lupus erythematosus

    Christian M Hedrich

    *Author for correspondence:

    E-mail Address: christian.hedrich@uniklinikum-dresden.de

    Pediatric Rheumatology & Immunology, Klinik und Poliklinik für Kinder- und Jugendmedizin, Universitätsklinikum Carl Gustav Carus, TU Dresden, Dresden, Germany

    ,
    Katrin Mäbert

    Pediatric Rheumatology & Immunology, Klinik und Poliklinik für Kinder- und Jugendmedizin, Universitätsklinikum Carl Gustav Carus, TU Dresden, Dresden, Germany

    ,
    Thomas Rauen

    Department of Nephrology & Clinical Immunology, RWTH University Hospital, Aachen, Germany

    &
    George C Tsokos

    Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA

    Published Online:https://doi.org/10.2217/epi-2016-0096

    Systemic lupus erythematosus (SLE) is a systemic autoimmune disease facilitated by aberrant immune responses directed against cells and tissues, resulting in inflammation and organ damage. In the majority of patients, genetic predisposition is accompanied by additional factors conferring disease expression. While the exact molecular mechanisms remain elusive, epigenetic alterations in immune cells have been demonstrated to play a key role in disease pathogenesis through the dysregulation of gene expression. Since epigenetic marks are dynamic, allowing cells and tissues to differentiate and adjust, they can be influenced by environmental factors and also be targeted in therapeutic interventions. Here, we summarize reports on DNA methylation patterns in SLE, underlying molecular defects and their effect on immune cell function. We discuss the potential of DNA methylation as biomarker or therapeutic target in SLE.

    Papers of special note have been highlighted as: • of interest; •• of considerable interest

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