*Joyce S. Hui-Yuen,1 Suhas K. Ganguli,1 James N. Jarvis2
1. Cohen Children’s Medical Center, Northwell Health and Hofstra-Northwell School of Medicine, New Hyde Park, New York, USA
2. Department of Pediatrics and Genetics, Genomics, & Bioinformatics Program,
Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA
*Correspondence to email@example.com
Disclosure: This work was supported, in part, by the Cohen Children’s Medical Center Mentored Pediatric Service Line Grant for Early Career Investigators (JSHY), a Delivering on Discovery grant from the Arthritis Foundation (JNJ), and a R01 grant (AR-060604) from the National Institutes of Health (JNJ).
Acknowledgements: We thank Dr Betty Diamond, Dr Clifford Deutschman, and Dr B. Anne Eberhard for their critical comments.
Received: 13.02.17 Accepted: 06.06.17
Citation: EMJ Rheumatol. 2017;4:90-97.
Systemic lupus erythematosus (SLE) is a chronic, multi-organ disease that predominantly affects young women of childbearing age. It is also a disease in which epigenetic modulation is emerging as an important mechanism for understanding how the environment interacts with inherited genes to produce disease. Much of the genetic risk for SLE identified in genome-wide association studies has been shown to lie in the non-coding genome, where epigenetic modifications of DNA and histone proteins regulate and co-ordinate transcription on a genome-wide basis. Novel methodologies, including high-throughput sequencing of open chromatin, RNA sequencing, protein microarrays, and gas chromatography-mass spectrometry, have revealed intriguing insights into the pathogenesis of SLE. We review these recent data and their potential contribution to more accurate diagnoses and the development of new therapeutic agents to improve patient outcomes.
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