R Hal Scofield

University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States

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Publications (240)1154.03 Total impact

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    ABSTRACT: The SSF Clinical Practice Guidelines are fully supported by the Sjo ̈ gren's Syndrome Foundation with no pharmaceutical support. No compensation was paid to any author. All participating authors completed Conflict of Interest forms of the American College of Rheumatology. Purpose: To improve quality of care for Sjo ̈ gren's (SS) systemic manifestations through consensus guidelines development. Methods: Of 97 clinical management questions for systemic manifestations identified from patient and rheumatologist surveys, 16 were selected for guideline development. The 1 st topics – Biologic use, DMARDS for treatment of MSK pain and Management of fatigue are presented. Each clinical question was developed in PICO format and assigned to a topic review group (TRG) which performed a systematic review, data extraction and drafted a guideline. Quality of evidence and strength of recommendation were rated using a modification of GRADE. Guideline recommendations were reviewed by a consensus expert panel comprised of 30–40 clinicians from academia and community practices as well as RNs and patients. A modified Delphi method was used with 75% agreement required. Of 1700 abstracts identified, 68 articles were reviewed. Results: Consensus was achieved for 20 recommendations; for 11 additional modalities, available data were insufficient to allow a recommendation to be formulated. Of the 20 recommendations, 18 required 1 Delphi round, 1 required 2 and 1 required 3. Key recommendations include a decision tree for the use of oral DMARDs for MSK pain with HCQ as first-line therapy, use of self-care measures and provision of advice regarding exercise to reduce fatigue and the use of HCQ in certain patient subsets (e.g inflammatory fatigue). The Clinical Practice Guidelines Committee (CPGC) recommended that the use of rituximab may be considered in specific clinical situations including vasculitis, severe parotid swelling, inflammatory arthritis, pulmonary disease and mononeuritis multiplex unresponsive to other therapies. The CPGC strongly discouraged the use of TNF alph inhibitors for sicca symptoms and for the majority of clinical contexts in primary SS. The CPGC updates its systematic reviews regularly and
    13th International Symposium on Sjogren's Syndrome, Bergen, Norway; 05/2015
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    ABSTRACT: Genetic variants at chromosomal region 11q23.3, near the gene ETS1, have been associated with systemic lupus erythematosus (SLE), or lupus, in independent cohorts of Asian ancestry. Several recent studies have implicated ETS1 as a critical driver of immune cell function and differentiation, and mice deficient in ETS1 develop an SLE-like autoimmunity. We performed a fine-mapping study of 14,551 subjects from multi-ancestral cohorts by starting with genotyped variants and imputing to all common variants spanning ETS1. By constructing genetic models via frequentist and Bayesian association methods, we identified 16 variants that are statistically likely to be causal. We functionally assessed each of these variants on the basis of their likelihood of affecting transcription factor binding, miRNA binding, or chromatin state. Of the four variants that we experimentally examined, only rs6590330 differentially binds lysate from B cells. Using mass spectrometry, we found more binding of the transcription factor signal transducer and activator of transcription 1 (STAT1) to DNA near the risk allele of rs6590330 than near the non-risk allele. Immunoblot analysis and chromatin immunoprecipitation of pSTAT1 in B cells heterozygous for rs6590330 confirmed that the risk allele increased binding to the active form of STAT1. Analysis with expression quantitative trait loci indicated that the risk allele of rs6590330 is associated with decreased ETS1 expression in Han Chinese, but not other ancestral cohorts. We propose a model in which the risk allele of rs6590330 is associated with decreased ETS1 expression and increases SLE risk by enhancing the binding of pSTAT1. Copyright © 2015 The American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.
    The American Journal of Human Genetics 04/2015; 96(5). DOI:10.1016/j.ajhg.2015.03.002 · 10.99 Impact Factor
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    ABSTRACT: Autoantibodies reactive with Ro52 are often found in sera of patients with Sjögren's syndrome (SS). This study was undertaken to investigate the role of Ro52-induced immune responses in pathogenesis of SS. New Zealand Mixed (NZM) 2758 mice were immunised with Ro52 in alum adjuvant. Control mice were immunised either with maltose-binding protein or injected with alum alone. Mice were monitored for anti-Ro52 antibody, sialoadenitis and pilocarpine-induced salivation. Antibody binding to salivary gland (SG) cells was analysed in vivo and in vitro by immunofluorescence. Sera from immunised mice were passively transferred into untreated or alum injected NZM2758 mice. By day 30 post-immunisation, Ro52 immunised mice generated immunoprecipitating anti-Ro52 antibodies and they had the maximum drop in saliva production. Both Ro52 immunised and control mice showed evidence of mild sialoadenitis. However, only Ro52 immunised mice had antibody deposition in their SG. Passive transfer of Ro52-immune sera induced SG dysfunction in recipient mice, only if the recipients were primed with alum. In vitro, antibodies from Ro52-immune sera were internalised by a SG cell line and this uptake was inhibited by cytochalasin D treatment. Our data show for the first time that antibodies induced by Ro52 are capable of inducing SG dysfunction, and that this phenomenon is dependent on the activation of innate immunity. The mouse model described in this study implies that autoantibody deposition in the SG might be an important step in the induction of xerostomia and pathogenesis of SS. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
    Annals of the Rheumatic Diseases 02/2015; DOI:10.1136/annrheumdis-2014-206297 · 9.27 Impact Factor
  • Biji T Kurien, Debashish Danda, R Hal Scofield
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    ABSTRACT: Dactyloscopy or fingerprint identification is a vital part of forensic evidence. Identification with fingerprints has been known since the finding of finger impressions on the clay surface of Babylonian legal contracts almost 4,000 years ago. The skin on the fingers and palms appears as grooves and ridges when observed under a microscope. A unique fingerprint is produced by the patterns of these friction skin ridges. Visible fingerprints can be deposited on solid surfaces. Colored inks have been used to deposit fingermarks on documents. Herein, we show that alkaline phosphatase can be used to transfer prints from fingers or palm to nitrocellulose or polyvinylidene difluoride membranes. The prints can be detected by using the nitro blue tetrazolium/5-bromo-4-chloro-3-indolyl phosphate method of detection.
    Methods in molecular biology (Clifton, N.J.) 01/2015; 1312:481-5. DOI:10.1007/978-1-4939-2694-7_50 · 1.29 Impact Factor
  • Biji T Kurien, R Hal Scofield
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    ABSTRACT: Proteins have been transferred from the gel to the membrane by a variety of methods. These include vacuum blotting, centrifuge blotting, electroblotting of proteins to Teflon tape and membranes for N- and C-terminal sequence analysis, multiple tissue blotting, a two-step transfer of low- and high-molecular-weight proteins, acid electroblotting onto activated glass, membrane-array method for the detection of human intestinal bacteria in fecal samples, protein microarray using a new black cellulose nitrate support, electrotransfer using square wave alternating voltage for enhanced protein recovery, polyethylene glycol-mediated significant enhancement of the immunoblotting transfer, parallel protein chemical processing before and during western blot and the molecular scanner concept, electronic western blot of matrix-assisted laser desorption/ionization mass spectrometric-identified polypeptides from parallel processed gel-separated proteins, semidry electroblotting of peptides and proteins from acid-urea polyacrylamide gels, transfer of silver-stained proteins from polyacrylamide gels to polyvinylidene difluoride (PVDF) membranes, and the display of K(+) channel proteins on a solid nitrocellulose support for assaying toxin binding. The quantification of proteins bound to PVDF membranes by elution of CBB, clarification of immunoblots on PVDF for transmission densitometry, gold coating of nonconductive membranes before matrix-assisted laser desorption/ionization tandem mass spectrometric analysis to prevent charging effect for analysis of peptides from PVDF membranes, and a simple method for coating native polysaccharides onto nitrocellulose are some of the methods involving either the manipulation of membranes with transferred proteins or just a passive transfer of antigens to membranes. All these methods are briefly reviewed in this chapter.
    Methods in molecular biology (Clifton, N.J.) 01/2015; 1312:487-503. DOI:10.1007/978-1-4939-2694-7_51 · 1.29 Impact Factor
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    ABSTRACT: An ultra-rapid method for electrophoresing proteins on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, transfer of proteins to nitrocellulose membranes, and immunoblotting is described here. Electrophoresis of the autoantigens La and Ro60, as well as molecular weight standards on a 4-20 % gradient gel, was performed in about 10 min using heated (70-75 °C) normal Laemmli running buffer. Electrophoretic transfer of these proteins was achieved in 7 min using a semidry transfer method. Finally, immunoblotting of La and Ro60 was carried out in 30 min. Thus, the entire process of electrophoresis, electrotransfer, and immunoblotting could be carried out in 1 h.
    Methods in molecular biology (Clifton, N.J.) 01/2015; 1312:449-54. DOI:10.1007/978-1-4939-2694-7_45 · 1.29 Impact Factor
  • Biji T Kurien, R Hal Scofield
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    ABSTRACT: Western blotting enables the detection and characterization of proteins of low abundance. Sodium dodecyl sulfate (SDS) polyacrylamide gel-separated proteins are normally transferred electrophoretically to nitrocellulose or polyvinylidene difluoride membranes. Here we describe the transfer proteins [Ro 60 (or SSA) autoantigen, 220 and 240 kDa spectrin antigens, and prestained molecular weight standards] by diffusion from SDS polyacrylamide gels at 37 °C. Up to 12 immunoblots can be obtained from a single gel by this method.
    Methods in molecular biology (Clifton, N.J.) 01/2015; 1312:77-86. DOI:10.1007/978-1-4939-2694-7_11 · 1.29 Impact Factor
  • Biji T Kurien, R Hal Scofield
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    ABSTRACT: A sensitive and specific method to analyze specific antibody clonotype changes in a lupus patient who developed autoantibodies to the Ro 60 autoantigen under observation is described. Patient sera, collected over several years, were separated by flatbed isoelectric focusing (IEF) and analyzed by affinity immunoblotting utilizing Ro 60-coated nitrocellulose membrane. When the Ro 60-coated nitrocellulose was laid over the surface of the IEF gel, the antibodies present on the surface of the acrylamide gel bound the Ro antigen on the nitrocellulose. Tween-20 was used to prevent nonspecific binding. The bound IgG clonotypes were detected using alkaline phosphatase conjugated anti-IgG. The patient's sera demonstrated an oligoclonal response to the Ro 60 autoantigen that increased in complexity and affinity over time.
    Methods in molecular biology (Clifton, N.J.) 01/2015; 1312:109-17. DOI:10.1007/978-1-4939-2694-7_15 · 1.29 Impact Factor
  • Biji T Kurien, R Hal Scofield
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    ABSTRACT: A method for the electrophoretic transfer of high and low molecular weight proteins to nitrocellulose membranes following sodium dodecyl sulfate (SDS) polyacrylamide gel is described here. The transfer was performed with heated (70-75 °C) normal transfer buffer from which methanol had been omitted. Complete transfer of high and low molecular weight antigens (molecular weight protein standards, a purified protein, and proteins from a human tissue extract) could be carried out in 10 min for a 7 % (0.75 mm) SDS polyacrylamide gel. For 10 and 12.5 % gels (0.75 mm) the corresponding time was 15 min. A complete transfer could be carried out in 20 min for 7, 10, and 12.5 % gels (1.5 mm gels). The permeability of the gel is increased by heat, such that the proteins trapped in the polyacrylamide gel matrix can be easily transferred to the membrane. The heat mediated transfer method was compared with a conventional transfer protocol, under similar conditions. The conventional method transferred minimal low molecular weight proteins while retaining most of the high molecular weight proteins in the gel. In summary, this procedure is particularly useful for the transfer of high molecular weight proteins, very rapid, and avoids the use of methanol.
    Methods in molecular biology (Clifton, N.J.) 01/2015; 1312:247-55. DOI:10.1007/978-1-4939-2694-7_26 · 1.29 Impact Factor
  • Biji T Kurien, R Hal Scofield
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    ABSTRACT: Western blotting is an important procedure for the immunodetection of proteins, particularly proteins that are of low abundance. This process involves the transfer of protein patterns from gel to microporous membrane. Electrophoretic as well as non-electrophoretic transfer of proteins to membranes was first described in 1979. Protein blotting has evolved greatly since the inception of this protocol, allowing protein transfer to be accomplished in a variety of ways.
    Methods in molecular biology (Clifton, N.J.) 01/2015; 1312:17-30. DOI:10.1007/978-1-4939-2694-7_5 · 1.29 Impact Factor
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    ABSTRACT: Background Sjögren’s Syndrome (SS) is characterized by dry eyes and dry mouth, mediated by inflammatory and lymphoproliferative components primarily affecting the exocrine glands. Serum antibodies to Ro and La as well as glandular infiltrates composed of antigen-experienced CD4+ T cells, CD27+ B cells and plasma cells (ASCs) are hallmarks of SS. In addition to anti-Ro and anti-La, antibodies to Sm and rheumatoid factor have also been found in the serum and saliva of SS patients. The purpose of our study was to interrogate the glandular ASC humoral immune response of SS patients and controls by producing fully human, monoclonal antibodies (hmAbs) from single cell-sorted minor salivary gland (SG) ASC infiltrates by determining and comparing their specificities. Methods Studies were approved by the OMRF and the University of Oklahoma Health Sciences Center Institutional Review Boards. Samples and data were obtained from 9 subjects following written, informed consent and evaluated in the OMRF Sjögren’s Research Clinic. Four subjects met American/European combined and American College of Rheumatology criteria for SS. One of these also met the American College of Rheumatology criteria for SLE. Five subjects that did not meet disease criteria served as sicca controls. ASCs were isolated from labial SGs by single-cell-sorting for hmAb production. hmAbs were produced by the OMRF Human Monoclonal Antibody Core. Serum Ab and hmAb profiles of patients and controls were evaluated by various assays to determine specificities including ELISA, immunofluorescence ANA and Crithidia luciliae testing, INNO-LIA™ and BioPlex2200™, and double immunodiffusion (sera only) assays. Results From the 72 hmAbs analyzed to date (52/patient; 20/control), we found diverse antigen specificities, with hmAbs from SS patients more often binding self-antigens. While 56% of the hmAbs from SS patients bound Ro and/or La, only 19% from sicca controls did (p =0.001). We found hmAbs from SS patients to be more often polyreactive (binding more than one antigen) than the controls (29% vs. 12%, respectively). In addition, 3 hmAbs were reactive to the bacterial antigen, peptidoglycan (PGN) (patient = 2, control = 1). The anti-PGN hmAbs also bound common self-antigens. We found correlation between patient serum and SG hmAbs specificities. Conclusion In this ongoing study, we show correlations between glandular and serum antibody specificities, demonstrate that ASCs other than anti-Ro or anti-La are present in SS salivary glands and produce Ab in situ. Furthermore, we observed that the SGs are representative of the systemic immune response and that glandular ASC specificities were consistent with co-morbid disease presentation. We have also identified SG derived hmAbs that have cross-reactivity to bacterial- and self-antigens, supporting the theory of an infection-triggering event that leads to development of disease. Finally, these are the first fully human, antigen-specific monoclonal antibodies produced from SS salivary gland ASCs and therefore, may have clinical or diagnostic importance.
    ACR 2014, Boston, MA, USA; 11/2014
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    ABSTRACT: Sjögren's syndrome (SS) is an autoimmune inflammatory disease that primarily affects the lacrimal and salivary glands causing dry eyes and mouth. Antibodies to Ro60 are frequently observed in patients with SS; however, the role of these antibodies in SS initiation and progression remains unclear. The sequence Ro60 273-289 (Ro274) is a known B cell epitope of Ro60and antibodies to this epitope have been observed in a subset of SS patients and in animals immunized with Ro60 protein. Animals immunized with Ro274 linear peptide develop a Sjögren's-like illness. We hypothesized that passive transfer of anti-Ro274-specific IgG would induce a Sjögren's-like phenotype. To evaluate this hypothesis, we adoptively transferred affinity-purified Ro274 antibodies into naïve BALB/c animals then evaluated salivary gland histology, function and IgG localization four days post-transfer. At this timepoint, there was no demonstrable mononuclear cell infiltration and salivary glands were histologically normal, but we observed a functional deficit in stimulated salivary flow of animals receiving Ro274 antibodies compared to animals receiving control IgG. Cellular fractionation and ELISA revealed Ro274-specific antibodies in the nucleus and cytoplasmic fractions of isolated parotid salivary gland cells that was confirmed by immunohistochemistry. These data support the hypothesis that antibodies to Ro274 deposit in salivary glands, can enter intact salivary gland cells and are involved in the dysregulation of salivary flow in SS.
    Clinical & Experimental Immunology 11/2014; 180(1). DOI:10.1111/cei.12480 · 3.28 Impact Factor
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    ABSTRACT: Exploiting genotyping, DNA sequencing, imputation, and trans-ancestral mapping, we used Bayesian and frequentist approaches to model the IRF5-TNPO3 locus association, now implicated in two immunotherapies and seven autoimmune diseases. Specifically, in systemic lupus erythematosus (SLE) we resolved separate associations in the IRF5 promoter (all ancestries) and with an extended European haplotype. We captured 3,230 IRF5-TNPO3 high quality, common variants across five ethnicities in 8,395 SLE cases and 7,367 controls. The genetic effect from the IRF5 promoter can be explained by any one of four variants in 5.7 kb (p-valuemeta=6x10(-49); OR=1.38-1.97). The second genetic effect spanned an 85.5 kb, 24 variant haplotype that included the genes IRF5 and TNPO3 (p-valuesEU=10(-27)-10(-32), OR=1.7-1.81). Many variants at the IRF5 locus with previously assigned biological function are not members of either final credible set of potential causal variants identified herein. In addition to the known biologically functional variants, we demonstrated that the risk allele of rs4728142, a variant in the promoter among the lowest frequentist probability and highest Bayesian posterior probability, was correlated with IRF5 expression and differentially binds the transcription factor ZBTB3. Our analytical strategy provides a novel framework for future studies aimed at dissecting etiological genetic effects. Finally, both SLE elements of the statistical model appear to operate in Sjögren's syndrome and systemic sclerosis while only the IRF5-TNPO3 gene-spanning haplotype is associated in primary biliary cirrhosis, demonstrating the nuance of similarity and difference in autoimmune disease risk mechanisms at IRF5-TNPO3.
    Human Molecular Genetics 09/2014; DOI:10.1093/hmg/ddu455 · 6.68 Impact Factor
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    ABSTRACT: Objectives The serologic hallmark of primary Sjögren’s syndrome (pSS) is IgG antibodies specific for Ro (SSA) and La (SSB). Molecular characteristics of glandular-derived B cells at the site of pSS inflammation have been described; however, parallels between glandular antibody-secreting cells (ASC) and serologic antibody specificities have not been evaluated. We utilized recombinant monoclonal antibody (hmAb) technology to study salivary gland-(SG) derived ASC specificities, evaluating their molecular characteristics and identified IgG antibody specificity.MethodshmAbs were generated from glandular IgG ASC. Heavy and light chain usage and immunoglobulin subclass were analyzed by sequencing. ELISA, indirect immunofluorescence, enzyme immunoassay and 35S immunoprecipitation analysis were used to determine antibody specificity.ResultsEvaluation of single ASCs from SG biopsies of patients with primary SS or with SS and overlapping SLE revealed significant concordance between serum autoantibody and glandular ASC specificities. Glandular-derived ASC heavy and light chains were extensively somatically hypermutated, indicative of antigen-driven responses. Specifically, we produced the first fully human monoclonal autoantibodies derived from salivary glands in this study.Conclusions Salivary glands in SS patients are a site for antibody production, which extend beyond the canonical Ro and/or La SS specificities. Furthermore, we demonstrate that glandular antibody production strongly reflects the serological humoral response in the two patients studied herein. © 2014 American College of Rheumatology.
    09/2014; DOI:10.1002/art.38872
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    ABSTRACT: Systemic lupus erythematosus (SLE; OMIM 152700) is characterised by the production of antibodies to nuclear antigens. We previously identified variants in complement receptor 2 (CR2/CD21) that were associated with decreased risk of SLE. This study aimed to identify the causal variant for this association.
    Annals of the Rheumatic Diseases 09/2014; DOI:10.1136/annrheumdis-2014-205584 · 9.27 Impact Factor
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    Robert Hal Scofield
    International Journal of Rheumatic Diseases 06/2014; 17(5). DOI:10.1111/1756-185X.12428 · 1.77 Impact Factor
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    ABSTRACT: In recent years, vitamin D has been shown to possess a wide range of immunomodulatory effects. Although there is extensive amount of research on vitamin D, we lack a comprehensive understanding of the prevalence of vitamin D deficiency or the mechanism by which vitamin D regulates the human immune system. This study examined the prevalence and correlates of vitamin D deficiency and the relationship between vitamin D and the immune system in healthy individuals. Healthy individuals (n = 774) comprised of European-Americans (EA, n = 470), African-Americans (AA, n = 125), and Native Americans (NA, n = 179) were screened for 25-hydroxyvitamin D [25(OH)D] levels by ELISA. To identify the most noticeable effects of vitamin D on the immune system, 20 EA individuals with severely deficient (<11.3 ng/mL) and sufficient (>24.8 ng/mL) vitamin D levels were matched and selected for further analysis. Serum cytokine level measurement, immune cell phenotyping, and phosphoflow cytometry were performed. Vitamin D sufficiency was observed in 37.5% of the study cohort. By multivariate analysis, AA, NA, and females with a high body mass index (BMI, >30) demonstrate higher rates of vitamin D deficiency (p<0.05). Individuals with vitamin D deficiency had significantly higher levels of serum GM-CSF (p = 0.04), decreased circulating activated CD4+ (p = 0.04) and CD8+ T (p = 0.04) cell frequencies than individuals with sufficient vitamin D levels. A large portion of healthy individuals have vitamin D deficiency. These individuals have altered T and B cell responses, indicating that the absence of sufficient vitamin D levels could result in undesirable cellular and molecular alterations ultimately contributing to immune dysregulation.
    PLoS ONE 04/2014; 9(4):e94500. DOI:10.1371/journal.pone.0094500 · 3.53 Impact Factor
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    ABSTRACT: Efforts to identify lupus-associated causal variants in the FAM167A/BLK locus on 8p21 are hampered by highly associated noncausal variants. In this report, we used a trans-population mapping and sequencing strategy to identify a common variant (rs922483) in the proximal BLK promoter and a tri-allelic variant (rs1382568) in the upstream alternative BLK promoter as putative causal variants for association with systemic lupus erythematosus. The risk allele (T) at rs922483 reduced proximal promoter activity and modulated alternative promoter usage. Allelic differences at rs1382568 resulted in altered promoter activity in B progenitor cell lines. Thus, our results demonstrated that both lupus-associated functional variants contribute to the autoimmune disease association by modulating transcription of BLK in B cells and thus potentially altering immune responses.
    The American Journal of Human Genetics 04/2014; 94(4):586-98. DOI:10.1016/j.ajhg.2014.03.008 · 10.99 Impact Factor
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    ABSTRACT: Objective: Primary Sjögren's syndrome (pSS) is a systemic autoimmune disease with incompletely understood etiology. Very little is known about the role of epigenetic dysregulation in the pathogenesis of pSS. Methods: We performed a genome-wide DNA methylation study in naïve CD4(+) T cells in eleven pSS patients compared to age-, sex-, and ethnicity-matched healthy controls. Cytosine methylation was quantified using the Illumina Infinium HumanMethylation450 BeadChip array and validated using bisulfite sequencing. Results: We identified 553 hypomethylated and 200 hypermethylated CpG sites in naïve CD4(+) T cells from pSS patients compared to healthy matched controls, representing 311 hypomethylated and 115 hypermethylated gene regions. Hypomethylated genes in pSS include LTA, coding for Lymphotoxin α. Other relevant genes such as CD247, TNFRSF25, PTPRC, GSTM1 and PDCD1 were also hypomethylated. The interferon signature pathway was represented by hypomethylation of STAT1, IFI44L, USP18 and IFITM1. A group of genes encoding for members of the solute carrier proteins were differentially methylated. In addition, the transcription factor RUNX1 was hypermethylated in patients, suggesting a possible connection to lymphoma predisposition. Gene ontology (GO) analysis of hypomethylated genes demonstrated enrichment of genes involved in lymphocyte activation and immune response. GO terms for hypermethylated genes included antigen processing and presentation. Conclusion: This is the first epigenome-wide DNA methylation study in pSS. Our data highlight a role for DNA methylation in pSS and identify disease-associated DNA methylation changes in several genes and pathways in naïve CD4(+) T cells in pSS that may be involved in the pathogenesis of this disease. © 2013 American College of Rheumatology.
    Arthritis & Rheumatology 03/2014; 66(3). DOI:10.1002/art.38264 · 7.87 Impact Factor

Publication Stats

6k Citations
1,154.03 Total Impact Points

Institutions

  • 1991–2015
    • University of Oklahoma Health Sciences Center
      • • College of Medicine
      • • Department of Biochemistry and Molecular Biology
      • • Section on Diabetes/Endocrinology
      Oklahoma City, Oklahoma, United States
  • 1999–2014
    • Oklahoma City University
      Oklahoma City, Oklahoma, United States
  • 1991–2014
    • Oklahoma Medical Research Foundation
      • Arthritis and Clinical Immunology Program
      Oklahoma City, Oklahoma, United States
  • 2013
    • Cincinnati Children's Hospital Medical Center
      • Division of Rheumatology
      Cincinnati, Ohio, United States
    • Medical University of South Carolina
      • Division of Rheumatology and Immunology
      Charleston, South Carolina, United States
  • 2012
    • University of Texas Southwestern Medical Center
      • Center for Cancer Immunobiology
      Dallas, Texas, United States
  • 2011
    • U.S. Department of Veterans Affairs
      Washington, Washington, D.C., United States
  • 1994–2001
    • University of Oklahoma
      Norman, Oklahoma, United States