Lihua Shi1, Zhe Zhang2, Li Song1, Yiu Tak Leung3, Michelle A Petri4, Kathleen E Sullivan1. 1. Division of Allergy & Immunology, The Children's Hospital of Philadelphia, 3615 Civic Center Boulevard, Philadelphia, PA 19104, USA. 2. The Center for Biomedical Informatics, The Children's Hospital of Philadelphia, Philadelphia, PA 1910, USA. 3. Division of Rheumatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. 4. Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Abstract
OBJECTIVE: Histone modifications set transcriptional competency and can perpetuate pathologic expression patterns. We defined systemic lupus erythematosus (SLE)-specific changes in H3K4me3 and K3K27me3, histone marks of gene activation and repression, respectively. METHODS: We used ChIP-seq to define histone modifications in monocytes from SLE patients and controls. RESULTS: Both promoters and enhancers exhibited significant changes in histone methylation in SLE. Regions with differential H3K4me3 in SLE were significantly enriched in potential interferon-related transcription factor binding sites and pioneer transcription factor sites. CONCLUSION: Enhancer activation defines the character of the cell and our data support extensive disease effects in monocytes, a particularly plastic lineage. Type I interferons not only drive altered gene expression but may also alter the character of the cell through chromatin modifications.
OBJECTIVE: Histone modifications set transcriptional competency and can perpetuate pathologic expression patterns. We defined systemic lupus erythematosus (SLE)-specific changes in H3K4me3 and K3K27me3, histone marks of gene activation and repression, respectively. METHODS: We used ChIP-seq to define histone modifications in monocytes from SLEpatients and controls. RESULTS: Both promoters and enhancers exhibited significant changes in histone methylation in SLE. Regions with differential H3K4me3 in SLE were significantly enriched in potential interferon-related transcription factor binding sites and pioneer transcription factor sites. CONCLUSION: Enhancer activation defines the character of the cell and our data support extensive disease effects in monocytes, a particularly plastic lineage. Type I interferons not only drive altered gene expression but may also alter the character of the cell through chromatin modifications.
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