ACR Meeting Abstracts

ACR Meeting Abstracts

  • Meetings
    • ACR Convergence 2024
    • ACR Convergence 2023
    • 2023 ACR/ARP PRSYM
    • ACR Convergence 2022
    • ACR Convergence 2021
    • ACR Convergence 2020
    • 2020 ACR/ARP PRSYM
    • 2019 ACR/ARP Annual Meeting
    • 2018-2009 Meetings
    • Download Abstracts
  • Keyword Index
  • Advanced Search
  • Your Favorites
    • Favorites
    • Login
    • View and print all favorites
    • Clear all your favorites
  • ACR Meetings

Abstracts tagged "interferons"

  • Abstract Number: 692 • 2012 ACR/ARHP Annual Meeting

    A Phase 1 Multicenter, Open-Label Study of MEDI-546, a Human Anti-Type I Interferon Receptor Monoclonal Antibody, in Adults with Scleroderma

    Avram Z. Goldberg1, Thomas D. Geppert2, Elena Schiopu3, Tracy M. Frech4, Vivien M. Hsu5, Robert W. Simms6, Stanford L. Peng7, Yihong Yao8, Nairouz Elgeioushi9, Bing Wang10, Linda Chang11 and Stephen Yoo12, 1Div of Rheumatology, North Shore-LIJ Health System, Lake Success, NY, 2Metroplex Clinical Research Center, LLC, Dallas, TX, 3Rheumatology/Internal Medicine, University of Michigan, Ann Arbor, MI, 4Internal Medicine-Division of Rheumatology, University of Utah School of Medicine, SLC, UT, 5Rheumatology, RWJ Med Schl Scleroderma Prog, New Brunswick, NJ, 6Rheumatology, Boston University School of Medicine, Boston, MA, 7Department of Rheumatology, Benaroya Research Institute at Virginia Mason Medical Center, Seattle, WA, 8Translational Sciences, MedImmune, Gaithersburg, MD, 9Medical Biostatistics, MedImmune, Gaithersburg, MD, 10Clinical Pharmacology and DMPK, Medimmune, Mountain View, CA, 11Translational Sciences, MedImmune, Hayward, CA, 12Clinical Development, MedImmune, Gaithersburg, MD

    Background/Purpose: Type I interferons (IFNs) have been implicated in the pathogenesis of scleroderma. This phase 1 study evaluated safety, pharmacokinetics (PK), pharmacodynamics, and immunogenicity of…
  • Abstract Number: 673 • 2012 ACR/ARHP Annual Meeting

    Altered Soluble Mediators in Individuals with Incomplete Lupus (ILE) in the Lupus Autoimmunity in Relatives (LAUREL) Study

    Melissa E. Munroe1, Jill M. Norris2, Joel M. Guthridge3, Diane L. Kamen4, Kathy Moser Sivils5, Timothy B. Niewold6, Gary S. Gilkeson7, Michael H. Weisman8, Mariko L. Ishimori8, Daniel J. Wallace9, David R. Karp10, John B. Harley11 and Judith A. James12, 1Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 2Epidemiology, Colorado School of Public Health, Aurora, CO, 3Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation, Oklahoma City, OK, 4Department of Medicine, Arthritis & Clinical Immunology Program, Oklahoma Medical Research Foundation, Charleston, SC, 5Oklahoma Medical Research Foundation, Oklahoma City, OK, 6Section of Rheumatology and Gwen Knapp Center for Lupus and Immunology Research, University of Chicago, Chicago, IL, 7Department of Medicine, Division of Rheumatology, Medical University of South Carolina, Charleston, SC, 8Rheumatology, Cedars-Sinai Medical Center, Los Angeles, CA, 9Cedars-Sinai Medical Center, Los Angeles, CA, 10Rheumatic Diseases Division, UT Southwestern Medical Center, Dallas, TX, 11Division of Rheumatology and The Center for Autoimmune Genomics & Etiology, University of Cincinnati, Cincinnati Children's Hospital Medical Center; US Department of Veterans Affairs Medical Center, Cincinnati, OH, 12Oklahoma Medical Research Foundation; University of Oklahoma Health Sciences Center, Oklahoma City, OK

    Background/Purpose: SLE is a complex autoimmune disease marked by autoantibody production and immune dysregulation. Identification of at-risk populations is essential to minimize morbidity and mortality…
  • Abstract Number: 680 • 2012 ACR/ARHP Annual Meeting

    Plasma Level of Galectin-3 Binding Protein Reflects Type I Interferon Activity and Is Highly Increased in Patients with Systemic Lupus Erythematosus

    Christoffer T. Nielsen1, Ole Østergaard2, Line V. Iversen3, Christian Lood4, Anders A. Bengtsson4, Anne Voss5, Søren Jacobsen6 and Niels H. H. Heegaard3, 1Department of Clinical Biochemistry, Immunology & Genetics, Statens Serum Institut, Copenhagen S, Denmark, 2Department of Clinical Biochemistry, Immunology & Genetics, Statens Serum Institute, Copenhagen S, Denmark, 3Department of Clinical Biochemistry, Immunology & Genetics, Statens Serum Institut, Copenhagen, Denmark, 4Department of Clinical Sciences, Section of Rheumatology, Lund University, Lund, Sweden, 5Dept of Rheumatology, Odense University Hospital, Odense C, Denmark, 6Department of Rheumatology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark

    Background/Purpose: Ongoing production of type I interferons (IFN) is a key element in the pathogenesis of systemic lupus erythematosus (SLE). Type I IFNs trigger the…
  • Abstract Number: 2687 • 2012 ACR/ARHP Annual Meeting

    Modular Microarray Analysis Fails to Reveal a Significant Biological Effect of Vitamin D3 Treatment in Patients Participating in a Double-Blind Randomized Placebo-Controlled Trial of the Effect of Vitamin D3 On the Interferon Signature in Patients with Systemic Lupus Erythematosus

    Michaela Oswald1, Cynthia Aranow2, Diane L. Kamen3, Meggan C. Mackay4, Ellen A. Goldmuntz5, Betty Diamond6, Peter K. Gregersen7 and ALE02 Study Team8, 1Laboratory of Genomics and Human Genetics, The Feinstein Institute for Medical Research, Manhasset, NY, 2Feinstein Institute for Medical Research, Manhasset, NY, 3Department of Medicine, Arthritis & Clinical Immunology Program, Oklahoma Medical Research Foundation, Charleston, SC, 4Autoimmune & Musculoskeletal Disease, The Feinstein Institute, Manhasset, NY, 5DAIT, NIAID/NIH, Bethesda, MD, 6Autoimmune & Musculoskeletal, Feinstein Institute Med Rsch, Manhasset, NY, 7Genomics and Human Genetics, Feinstein Institute for Medical Research, Manhasset, NY, 8NIAID/NIH Rm 6807, Bethesda, MD

    Background/Purpose: Vitamin D modulates the immune response. Exposing normal PBMCs to activating SLE sera induces an interferon signature which can be inhibited by preexposure of…
  • Abstract Number: 2677 • 2012 ACR/ARHP Annual Meeting

    IL-23 Controls Autoimmunity by Facilitating Clearance of Apoptotic Bodies in the Marginal Zone in Lupus-Prone BXD2 Mice

    Hao Li1, Hui-Chen Hsu2, Qi Wu3, PingAr Yang3, Jun Li4, Daniel Cua5, Mohamed Oukka6 and John D. Mountz7, 1Microbiology, University of Alabama at Birmingham, Birmingham, AL, 2Department of Medicine, Clinical Immunology & Rheumatology, University of Alabama at Birmingham, Birmingham, AL, 3Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, 4Med - Immunology/Rheumatology, University of Alabama at Birmingham, Birmingham, AL, 5Discovery Research, Merck Research Laboratory, Palo Alto, CA, 6Pediatrics, Seattle, WA, 7Dept of Med/Rheumatology Div, University of Alabama at Birmingham, Birmingham, AL

    Background/Purpose: Failure to clear apoptotic bodies is a central pathogenic mechanism for SLE. We have observed that spontaneous systemic autoimmunity and lupus in BXD2 mice…
  • Abstract Number: 2619 • 2012 ACR/ARHP Annual Meeting

    A Double-Blind Randomized Placebo-Controlled Trial of the Effect of Vitamin D3 On the Interferon Signature in Patients with Systemic Lupus Erythematosus

    Cynthia Aranow1, Maria Dall'era2, Elena M. Massarotti3, Meggan C. Mackay4, Andreea Coca5, Fotios Koumpouras6, Marc C. Levesque7, W. Winn Chatham8, Megan E. B. Clowse9, Lisa G. Criscione-Schreiber10, Sherri Callahan11, Ellen A. Goldmuntz12, Lynette Keyes-Elstein13, Betty Diamond14 and Diane L. Kamen15, 1Feinstein Institute for Medical Research, Manhasset, NY, 2Medicine/Rheumatology, University of California, San Francisco, San Francisco, CA, 3Rheumatology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 4Autoimmune & Musculoskeletal Disease, The Feinstein Institute, Manhasset, NY, 5Allergy, Immunology and Rheumatology, University of Rochester, Rochester, NY, 6Lupus Center of Excellence, West Penn Hospital, Pittsburgh, PA, 7Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA, 8University of Alabama at Birmingham, Birmingham, AL, 9Rheumatology, Duke University Medical Center, Durham, NC, 10Rheumatology, Duke University Health System, Durham, NC, 11Dait, NIAID/NIH Rm 6807, Bethesda, MD, 12DAIT, NIAID/NIH, Bethesda, MD, 13Rho Federal Systems, Inc., Chapel Hill, NC, 14Autoimmune & Musculoskeletal, Feinstein Institute Med Rsch, Manhasset, NY, 15Department of Medicine, Arthritis & Clinical Immunology Program, Oklahoma Medical Research Foundation, Charleston, SC

    Background/Purpose: Exposure of normal PBMCs to1,25 OH vitamin D reverses the stimulatory effects of activating SLE sera on the interferon signature.  Given that IFN is…
  • Abstract Number: 2653 • 2012 ACR/ARHP Annual Meeting

    A Subset of up-Regulated IFN Regulated Genes in Candle Patients Decrease with Treatment with a JAK Inhibitor

    Adriana Almeida de Jesus1, Yin Liu2, Gina A. Montealegre3, Adam L. Reinhardt4, Diane Brown5, Antonio Torrelo6, Angel V. Casano7, Lena Das8, Yongqing Chen9, Yan Huang9, Deborah Stone10, Dawn C. Chapelle2, Nicole Plass2, Steven H. Zuckerman11, William Macias12 and Raphaela T. Goldbach-Mansky2, 1Translational Autoinflammatory Disease Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, MD, 2Translational Autoinflammatory Diseases Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, MD, 3NIAMS, Bethesda, MD, 4Rheumatology, Children's Hosp of Omaha/UNMC, Omaha, NE, 5Division Of Rheumatology MS #60, Children's Hospital Los Angeles, Los Angeles, CA, 6Departments of Pediatric Dermatology, Hospital Niño Jesús, Madrid, Spain, Madrid, Spain, 7Meditex Spain, Malaga, Spain, 8Pediatric Rheumatology, KK Women's and Children's Hospital, Singapore, Singapore, 9Translational Autoinflammatory Disease Section, Office of the Clinical Director NIAMS, Bethesda, MD, 10National Institute of Arthritis & Muscoloskeletal, National Institutes of Health, Bethesda, MD, 11Immunology, Lilly Research Labs, Indianapolis, IN, 12Eli Lilly and Company, Indianapolis, IN

    Background/Purpose: Chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature (CANDLE) syndrome is a recently described early-onset autoinflammatory disease caused by autosomal recessive mutations in…
  • Abstract Number: 2124 • 2012 ACR/ARHP Annual Meeting

    Serum Concentrations of Soluble Interferon Receptor in Patients with Rheumatoid Arthritis

    Masao Sato1, Masao Takemura2, Ryuki Shinohe3, Tsuneo Watanabe2 and Katsuji Shimizu3, 1Rheumatology, Matsunami General Hospital, Gifu, Japan, 2Informative Clinical Medicine, Gifu University, Gifu, Japan, 3Orthopaedic Surgery, Gifu University, Gifu, Japan

    Background/Purpose: Interferon (IFN) exerts antiviral and antineoplastic activities, and is involved in immunoregulatory activities. IFN probably plays an important role in the pathogenesis of rheumatoid…
  • Abstract Number: 1811 • 2012 ACR/ARHP Annual Meeting

    On the Origin of the Type I Interferon Signature in Rheumatoid Arthritis

    T.D. de Jong1, Saskia Vosslamber1, Maija-Leena Eloranta2, Lars Rönnblom2, Kyra Gelderman1, Mary von Blomberg1, Irene Bultink3, Alexandre Voskuyl4 and Cornelis L. Verweij1, 1Pathology, VU University Medical Center, Amsterdam, Netherlands, 2Department of Medical Sciences, Section of Rheumatology, Uppsala University, Uppsala, Sweden, 3Department of Rheumatology, VU University Medical Center, Amsterdam, Netherlands, 4Rheumatology, VU University Medical Center, Amsterdam, Netherlands

    Background/Purpose: Presence of a type I interferon (IFN) signature has been described for several autoimmune diseases, including systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).…
  • Abstract Number: 1791 • 2012 ACR/ARHP Annual Meeting

    Different Mechanisms Responsible for IVIG Inhibition of Immune Complex Versus TLR Stimulated Interferon-Alpha

    Alice Wiedeman1, Fabian Käsermann2, Sylvia Miescher2 and Keith B. Elkon3, 1Department of Immunology, University of Washington, Seattle, WA, 2CSL Behring, Bern, Switzerland, 3Rheumatology Box 356428, University of Washington, Seattle, WA

    Background/Purpose:   SLE immune complexes (IC) induce IFN-α production by stimulation of TLR7 and 9 in plasmacytoid dendritic cells (pDC).  Serum from normal human donors…
  • Abstract Number: 1440 • 2012 ACR/ARHP Annual Meeting

    Lupus-Prone Mice Demonstrate Enhanced Neutrophil Extracellular Trap Formation: Implications for Autoantibody Formation and Organ Damage

    Jason S. Knight1, Alexander A. O'Dell1, Wenpu Zhao2, Ritika Khandpur2, Srilakshmi Yalavarthi2 and Mariana J. Kaplan3, 1Department of Internal Medicine, Division of Rheumatology, University of Michigan, Ann Arbor, MI, 2University of Michigan Rheumatology, Ann Arbor, MI, 3Systemic Autoimmunity Branch, National Institutes of Health/NIAMS, Bethesda, MD

    Background/Purpose: Recent evidence suggests that enhanced neutrophil extracellular trap (NET) formation—the programmed release of chromatin fibers decorated with granular antimicrobial peptides—is as an important activator…
  • Abstract Number: 1446 • 2012 ACR/ARHP Annual Meeting

    The Granulocyte Signature and Organ Inflammation in TLR7 Responsive Mice Is RNA and Type 1 Interferon Dependent

    Xizhang Sun1, Alice Wiedeman2, Thomas H. Teal3, Nalini Agrawal3, Jeffrey Duggan2, Matt B. Buechler4, Jeffrey A. Ledbetter3, Denny Liggitt5, Jessica A. Hamerman6 and Keith B. Elkon7, 1Division of Rheumatology, University of Washington, Seattle, WA, 2Department of Immunology, University of Washington, Seattle, WA, 3Rheumatology, University of Washington, Seattle, WA, 4Benaroya Research Institute at Virginia Mason, Seattle, WA, Seattle, 5Comparative Medicine, University of Washington, Seattle, WA, 6Benaroya Research Institute at Virginia Mason, Seattle, WA, 7Rheumatology Box 356428, University of Washington, Seattle, WA

    Background/Purpose: Microarray expression analysis of blood taken from patients with Systemic Lupus Erythematosus (SLE) has revealed two characteristic signatures: one that reflects exposure to type…
  • Abstract Number: 1067 • 2012 ACR/ARHP Annual Meeting

    Spontaneous Aggregation of the Anti-Viral Mavs Protein in Certain Systemic Lupus Erythematosus Patients May Explain Excessive Type I Interferon Production

    Philip L. Cohen1 and Wen-Hai Shao2, 1Rheumatology, Temple University, Philadelphia, PA, 2Medicine, Temple University School of Medicine, Philadelphia, PA

    Background/Purpose: Patients with systemic lupus (SLE) often have increased type I interferon levels (IFN-I) and activation of IFN-inducible genes (IFN signature).  The mitochondrial adaptor protein…
  • Abstract Number: 880 • 2012 ACR/ARHP Annual Meeting

    Interferon Regulatory Factor 8 Regulates BAFF Production in Murine Macrophages and Is a Nexus for Cross Talk Between IFN-γ and TGF-β

    Weijia Yuan1, Sanjay Gupta2, Jane E. Salmon3 and Alessandra B. Pernis2, 1Rheumatology, Hospital for Special Surgery, Weill Cornell Medical College, New York, NY, 2Autoimmunity & Inflammation, Hospital for Special Surgery, Weill Cornell Medical College, New York, NY, 3Dept of Medicine, Hospital for Special Surgery, Weill Cornell Medical College, New York, NY

    Background/Purpose: Lupus is a systemic autoimmune disease that can lead to severe end-organ damage characterized by unabated inflammation and aberrant tissue repair. Macrophage dysregulation plays…
  • Abstract Number: 885 • 2012 ACR/ARHP Annual Meeting

    Interferon α and Self-Organized Criticality Theory

    Shunichi Shiozawa1, Yumi Miyazaki2 and Ken Tsumiyama3, 1Department of Medicine, Kyushu University Beppu Hospital, Beppu, Japan, 2Kyushu University Beppu Hospital/ Kobe University Graduate School of Health Sciences, Beppu/ Kobe, Japan, 3Department of Rheumatology, Kyushu University Beppu Hospital, Beppu, Japan

    Background/Purpose: One of the biggest obstacle we face in elucidating the pathogenesis of autoimmunity today is the mechanism how autoreactive lymphocyte clones could survive or…
  • « Previous Page
  • 1
  • …
  • 7
  • 8
  • 9
  • 10
  • Next Page »
Advanced Search

Your Favorites

You can save and print a list of your favorite abstracts during your browser session by clicking the “Favorite” button at the bottom of any abstract. View your favorites »

All abstracts accepted to ACR Convergence are under media embargo once the ACR has notified presenters of their abstract’s acceptance. They may be presented at other meetings or published as manuscripts after this time but should not be discussed in non-scholarly venues or outlets. The following embargo policies are strictly enforced by the ACR.

Accepted abstracts are made available to the public online in advance of the meeting and are published in a special online supplement of our scientific journal, Arthritis & Rheumatology. Information contained in those abstracts may not be released until the abstracts appear online. In an exception to the media embargo, academic institutions, private organizations, and companies with products whose value may be influenced by information contained in an abstract may issue a press release to coincide with the availability of an ACR abstract on the ACR website. However, the ACR continues to require that information that goes beyond that contained in the abstract (e.g., discussion of the abstract done as part of editorial news coverage) is under media embargo until 10:00 AM ET on November 14, 2024. Journalists with access to embargoed information cannot release articles or editorial news coverage before this time. Editorial news coverage is considered original articles/videos developed by employed journalists to report facts, commentary, and subject matter expert quotes in a narrative form using a variety of sources (e.g., research, announcements, press releases, events, etc.).

Violation of this policy may result in the abstract being withdrawn from the meeting and other measures deemed appropriate. Authors are responsible for notifying colleagues, institutions, communications firms, and all other stakeholders related to the development or promotion of the abstract about this policy. If you have questions about the ACR abstract embargo policy, please contact ACR abstracts staff at [email protected].

Wiley

  • Online Journal
  • Privacy Policy
  • Permissions Policies
  • Cookie Preferences

© Copyright 2025 American College of Rheumatology