Answers are grounded in this paper and cite their sources.
Systemic lupus erythematous (SLE) is characterized by the body's lack of distinction between self- and nonself-antigens amounting to hyperactive immune reactions. In most cases, this type of autoimmune disorder has no exact known causal factor and can be caused by both genetic and epigenetic influences. One of the major points of interest in SLE research is understanding the disease biology from a wide landscape involving both the genome and epigenome of SLE patients. Availability of high-throughput gene sequencing, genome-wide association studies, and gene enrichment analysis has facilitated our understanding of the pathogenesis of SLE. However, the correlation of these genetic and epigenetic changes is still poorly understood, and therefore, this review makes a first overarching attempt to bridge the existing gap in the scientific domain.
No takes yet. Share an insight, caveat, or question.
A 2016 study studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: