PURPOSE OF REVIEW: Systemic lupus erythematosus is a severe 
autoimmune/inflammatory condition of unknown pathophysiology. Though genetic 
predisposition is essential for disease expression, risk alleles in single genes 
are usually insufficient to confer disease. Epigenetic dysregulation has been 
suggested as the missing link between genetic risk and the development of 
clinically evident disease.
RECENT FINDINGS: Over the past decade, epigenetic events moved into the focus of 
research targeting the molecular pathophysiology of SLE. Epigenetic alteration 
can be the net result of preceding infections, medication, diet, and/or other 
environmental influences. While altered DNA methylation and histone 
modifications had already been established as pathomechanisms, DNA 
hydroxymethylation was more recently identified as an activating epigenetic 
mark. Defective epigenetic control contributes to uncontrolled cytokine and 
co-receptor expression, resulting in immune activation and tissue damage in SLE. 
Epigenetic alterations promise potential as disease biomarkers and/or future 
therapeutic targets in SLE and other autoimmune/inflammatory conditions.