title: Expression and methylation data from SLE patient and healthy control blood samples subdivided with respect to ARID3a levels.
abstract: Previously published studies revealed that variation in expression of the DNA-binding protein ARID3a in B lymphocytes from patients with systemic lupus erythematosus (SLE) correlated with levels of disease activity ("Disease activity in systemic lupus erythematosus correlates with expression of the transcription factor AT-rich-interactive domain 3A" (J.M. Ward, K. Rose, C. Montgomery, I. Adrianto, J.A. James, J.T. Merrill et al., 2014) [1]). The data presented here compare DNA methylation patterns from SLE peripheral blood mononuclear cells obtained from samples with high numbers of ARID3a expressing B cells (ARID3a(H)) versus SLE samples with normal numbers of ARID3a(+) B cells (ARID3a(N)). The methylation data is available at the gene expression omnibus (GEO) repository, "Gene Expression Omnibus: NCBI gene expression and hybridization array data repository" (R. Edgar, M. Domrachev, A.E. Lash, 2002) [2]. Isolated B cells from SLE ARID3a(H) and ARID3a(N) B samples were also evaluated via qRT-PCR for Type I interferon (IFN) signature and pathway gene expression levels by qRT-PCR. Similarly, healthy control B cells and B cells stimulated to express ARID3a with the TLR agonist, CpG, were also compared via qRT-PCR. Primers designed to detect 6 IFNa subtype mRNAs were tested in 4 IFNa, Epstein-Barr Virus-transformed B cell lines ("Reduced interferon-alpha production by Epstein-Barr virus transformed B-lymphoblastoid cell lines and lectin-stimulated lymphocytes in congenital dyserythropoietic anemia type I" (S.H. Wickramasinghe, R. Hasan, J. Smythe, 1997) [3]). The data in this article support the publication, "Human effector B lymphocytes express ARID3a and secrete interferon alpha" (J.M. Ward, M.L. Ratliff, M.G. Dozmorov, G. Wiley, J.M. Guthridge, P.M. Gaffney, J.A. James, C.F. Webb, 2016) [4].
authors.affiliation: Department of Medicine, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma, USA.
authors.forename: Julie M
authors.initials: JM
authors.lastname: Ward
authors.affiliation: Department of Medicine, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma, USA.
authors.forename: Michelle L
authors.initials: ML
authors.lastname: Ratliff
authors.affiliation: Department of Biostatistics, Virginia Commonwealth University, Richmond, Virginia, USA.
authors.forename: Mikhail G
authors.initials: MG
authors.lastname: Dozmorov
authors.affiliation: Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
authors.forename: Graham
authors.initials: G
authors.lastname: Wiley
authors.affiliation: Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
authors.forename: Joel M
authors.initials: JM
authors.lastname: Guthridge
authors.affiliation: Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
authors.forename: Patrick M
authors.initials: PM
authors.lastname: Gaffney
authors.affiliation: Department of Medicine, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma, USA; Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA; Department of Pathology, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma, USA.
authors.forename: Judith A
authors.initials: JA
authors.lastname: James
authors.affiliation: Department of Medicine, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma, USA; Department of Microbiology and Immunology, Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA; Department of Cell Biology, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma, USA.
authors.forename: Carol F
authors.initials: CF
authors.lastname: Webb
keywords: ARID3a; B cells; SLE