Introduction: Systemic Lupus Erythematosus (SLE) is a multi-dimensional autoimmune disease involving numerous tissues throughout the body. The chromatin accessibility landscapes in immune cells play a pivotal role in governing their activation, function, and differentiation. Aberrant modulation of chromatin accessibility in immune cells is intimately associated with the onset and progression of SLE.
Areas covered: In this review, we described the chromatin accessibility landscapes in immune cells, summarized the recent evidence of chromatin accessibility related to the pathogenesis of SLE, and discussed the potential of chromatin accessibility as a valuable option to identify novel therapeutic targets for this disease.
Expert opinion: Dynamic changes in chromatin accessibility are intimately related to the pathogenesis of SLE and have emerged as a new direction for exploring its epigenetic mechanisms. The differently accessible chromatin regions in immune cells often contain binding sites for transcription factors (TFs) and cis-regulatory elements such as enhancers and promoters, which may be potential therapeutic targets for SLE. Larger scale cohort studies and integrating epigenomic, transcriptomic, and metabolomic data can provide deeper insights into SLE chromatin biology in the future.
Keywords: Systemic lupus erythematosus; chromatin accessibility; epigenetic; immune cells; immune regulation.
Recently, there has been a growing body of studies that explore the influence of epigenetic factors including DNA methylation, histone post-translational modifications, and non-coding RNA regulation on Systemic Lupus Erythematosus (SLE). Unusual regulation of these common epigenetic modifications would change the chromatin accessibility landscapes in SLE immune cells. Many studies have mapped the chromatin accessibility of various immune cells in SLE patients to uncover potential regulators like transcription factors (TFs) and cis-regulatory elements. Higher chromatin accessibility of immune cells in SLE patients compared to healthy individuals provides new avenues for diagnosing this disease. TFs identified in differentially accessible chromatin regions and their regulated genes might serve as novel targets for therapies, where the phenotypes affected by these genes, like inflammatory cytokine release and immune activation, are reliable bases for evaluating the prognosis of such targeted therapies.In this review, we described the chromatin accessibility landscape in immune cells, summarized the recent evidence of chromatin accessibility related to the process by which SLE develops, and discussed the potential of chromatin accessibility as a valuable option to identify novel therapeutic targets for this disease. Larger scale studies and combining epigenomic, transcriptomic, and metabolomic data can provide deeper insights into SLE chromatin biology in the future.