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Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disorder that is characterized by autoantibody production and dysregulated immune cell activation. Although the exact etiology of SLE remains unknown, genetic, hormonal, and complex environmental factors are known to be critical for pathologic immune activation. In addition to the inherited genetic predisposition, epigenetic processes that do not change the genomic code, such as DNA methylation, histone modification, and noncoding RNAs are increasingly appreciated to play important roles in lupus pathogenesis. We herein focus on the up-to-date findings of lupus-associated epigenetic alterations and their pathophysiology in lupus development. We also summarize the therapeutic potential of the new findings. It is likely that advances in the epigenetic study will help to predict individual disease outcomes, promise diagnostic accuracy, and design new target-directed immunotherapies.
Highlights
Systemic lupus erythematosus (SLE) is a female predominant autoimmune disorder characterized by autoantibody production and organ damages due to immune complex-mediated pathology [1]
A total of 22 CpG sites in the promoter and enhancer regions of the CD40 ligand gene (CD40L) were investigated for their functional association with the disease activity presented in 49 female SLE patients [19]
The DNA methylation status (~460,000 CpG sites) of B cells in various development stages was examined in AA and European American (EA) SLE patients [43]
Summary
Systemic lupus erythematosus (SLE) is a female predominant autoimmune disorder characterized by autoantibody (autoAb) production and organ damages due to immune complex-mediated pathology [1]. In SLE development, it is believed that reoccurring environmental factors trigger proinflammatory responses in individuals with genomic and epigenomic susceptibility. Under such persistent inflammatory conditions, loss of the central and peripheral immunological tolerance leads to the clinical manifestation of SLE. MicroRNAs (miRNAs) are noncoding small RNAs that act as epigenetic modulators to regulate the protein levels of target mRNAs without modifying the genetic sequences. Those inheritable changes are independent of the genomic DNA sequence.
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