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- Study Description
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- Data Use Certification (DUC) Agreement
- Talking Glossary of Genetic Terms
Background: Systemic lupus erythematosus (SLE) is an autoimmune disease with protean manifestations. This study identifies two histone marks of activation and the binding of p300 genome-wide in three cell types and three clinical subsets to better understand cell-specific effects and differences across clinical subsets.
Results: We examined 20 patients with SLE and 8 controls and found the TNF, IL-2/STAT5, and KRAS pathways were identified across multiple cell types and ChIP data sets. Patients with cutaneous lupus and lupus nephritis generally had less dramatically altered chromatin than the general SLE group.
Conclusions: NFkB and classical inflammatory pathways were strongly associated with increased peak heights across all cell types but were the highest-ranking pathway for all three antibodies in monocytes according to fgsea analysis. IL-6 Jak/STAT3 signaling was the most significant pathway association in T cells marked by H3K27ac change. Therefore, each cell type experiences the disease process distinctly although in all cases there was a strong theme of classical inflammatory pathways. These studies define important cell type differences and emphasize the breadth of the inflammatory effects in SLE.
- Study Design:
- Case-Control
- Study Type:
- Case-Control
- Total number of consented subjects: 28
- Subject Sample Telemetry Report (SSTR)
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- Publicly Available Data
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- Study Inclusion/Exclusion Criteria
Inclusion Criteria:
Adult females with SLE or without (healthy controls).
- Selected Publications
- Diseases/Traits Related to Study (MeSH terms)
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- Primary Phenotype: Lupus Erythematosus, Systemic
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- Study Attribution
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Principal Investigator
- Kathleen E. Sullivan. Division of Allergy Immunology, Department of Pediatrics, Children’s Hospital of Philadelphia, Philadelphia, PA, USA.
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Co-Investigators
- Katherine Beigel. Department of Biomedical and Health Informatics, Children's Hospital of Philadelphia Research Institute, Abramson Research Center, Philadelphia, PA, USA.
- Xiao Min Wang. Division of Allergy Immunology, Department of Pediatrics, Children’s Hospital of Philadelphia, Philadelphia, PA, USA.
- Li Song. Division of Allergy Immunology, Department of Pediatrics, Children’s Hospital of Philadelphia, Philadelphia, PA, USA.
- Kelly Maurer. Division of Allergy Immunology, Department of Pediatrics, Children’s Hospital of Philadelphia, Philadelphia, PA, USA.
- Christopher Breen. Division of Allergy Immunology, Department of Pediatrics, Children’s Hospital of Philadelphia, Philadelphia, PA, USA.
- Deanne Taylor. Department of Biomedical and Health Informatics, Children's Hospital of Philadelphia Research Institute, Abramson Research Center, Philadelphia, PA, USA; Department of Pediatrics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.
- Daniel Goldman. Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
- Michelle Petri. Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
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Principal Investigator