ACR Meeting Abstracts

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Abstracts tagged "synovial fluid and tumor necrosis factor (TNF)"

  • Abstract Number: 1117 • 2016 ACR/ARHP Annual Meeting

    EGCG Down-Regulates TNF-α-Induced Mcl-1 Expression By Modulating Mule/Huwe1, β-TrCP, and USP9X Ubiquitin/De-Ubiquitin Ligases in Rheumatoid Arthritis Synovial Fibroblasts

    Nahid Akhtar1, Sadiq Umar2, David Fox3 and Salahuddin Ahmed1, 1Department of Pharmaceutical Sciences, Washington State University, College of Pharmacy, Spokane, WA, 2Department of Pharmaceutical Science, Washington State University, College of Pharmacy, Spokane, WA, 3Department of Medicine [Division of Rheumatology], University of Michigan, Ann Arbor, MI

    Background/Purpose:   Myeloid cell leukemia (Mcl-1) phosphorylation at Ser64 position (p-Mcl-1Ser64) has been shown to enhance Mcl-1’s stability and resistance to proteasomal degradation. However, the…
  • Abstract Number: 2557 • 2016 ACR/ARHP Annual Meeting

    Tumor Necrosis Factor (TNF) Sensitizes Rheumatoid Synovial Fibroblasts to TRPA1-Mediated Calcium Flux, Anti-Proliferation and Cell Death

    Torsten Lowin1, Rainer Straub2 and Georg Pongratz3, 1Rheumatology, University Hospital Duesseldorf, Duesseldorf, Germany, 2Laboratory of Experimental Rheumatology and Neuroendocrine Immunology, Department of Internal Medicine, University Hospital Regensburg, Regensburg, Germany, 3Rheumatology - Hiller Research Center Rheumatology, University Hospital Duesseldorf, Duesseldorf, Germany

    Background/Purpose:  In rheumatoid arthritis (RA), synovial fibroblasts (SF) are one main contributor of joint destruction since they resist apoptosis and secrete pro-inflammatory cytokines and matrix…
  • Abstract Number: 2447 • 2014 ACR/ARHP Annual Meeting

    The Role of TET3-Mediated DNA Demethylation By Pro-Inflammatory Cytokines in Rheumatoid Arthritis

    Kazuhisa Nakano1, Kunihiro Yamaoka1, Akira Kurozumi2, Akio Kawabe2, Kaoru Yamagata2 and Yoshiya Tanaka3, 1The First Department of Internal Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan, 2The first department of Internal Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan, 3University of Occupational and Environmental Health, Japan, Kitakyushu, Japan

    Background/Purpose In the pathogenesis of Rheumatoid arthritis (RA) RA fibroblast-like synoviocytes (RA FLS) exhibit a unique aggressive phenotype that contributes to the cytokine milieu and…
  • Abstract Number: 1042 • 2014 ACR/ARHP Annual Meeting

    IL-1β and TNF-α Promote Monocyte Viability through the Induction of GM-CSF Expression By Rheumatoid Arthritis Synovial Fibroblasts

    Christelle Darrieutort-Laffite1,2, Marie Astrid Boutet1, Mathias Chatelais1, Regis Brion3, Frederic Blanchard1, Dominique Heymann3 and Benoit Le Goff1,2, 1Laboratoire de Physiopathologie de la Résorption Osseuse et Thérapie des Tumeurs Osseuses Primitives, INSERM, UMR 957, Nantes, France, 2Rheumatology, Nantes University Hospital, Nantes, France, 3Laboratoire de Physiopathologie de la Résorption Osseuse et Thérapie des Tumeurs Osseuses Primitives, Nantes, INSERM, UMR 957, Nantes, France

    Background/Purpose Macrophages and synovial fibroblasts (SF) are two major cells implicated in the pathogenesis of rheumatoid arthritis (RA). They can interact in the synovial micro-environment…
  • Abstract Number: 1001 • 2014 ACR/ARHP Annual Meeting

    Fibroblast-like Synoviocytes Inhibit Wnt Signaling Pathway By Secreting Dockcop-1

    Satoshi Yamasaki and Eiji Sugiyama, Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital, Hiroshima, Japan

    Background/Purpose: There is evidence of osteoclast activation in the inflamed joints of patients with rheumatoid arthritis (RA). Studies that focus on osteoblasts are not sufficient…
  • Abstract Number: 1856 • 2013 ACR/ARHP Annual Meeting

    Potentiating Effects Of IL-17A, IL-17AF, IL-17F In Combination With TNF But Not With IL-1beta In Human Primary Fibroblast-Like Synoviocytes From Rheumatoid Arthritis Patients

    Christine Huppertz1, Marija Curcic Djuric1, Robert Hennze1, Friedrich Raulf1, Frank Kolbinger1, Anis Mir1 and David Lee2, 1Autoimmunity, Transplantation and Inflammatory Disease, Novartis Institutes for BioMedical Research, Novartis Pharma AG, Basel, SWITZERLAND, Basel, Switzerland, 2Novartis Pharma AG, Basel, Switzerland

    Background/Purpose: The pro-inflammatory cytokine interleukin-17A (IL-17A) activates fibroblast-like synoviocytes (FLS) and other mesenchymal cells via the IL-17RA/RC receptor. FLS are a major source of inflammatory…
  • Abstract Number: 951 • 2013 ACR/ARHP Annual Meeting

    The Anti-IL-17A Monoclonal Antibody Secukinumab (AIN457) Inhibits Pro-Inflammatory Mediator Release From Human Primary Synoviocytes Costimulated With IL-17 and TNF

    Christine Huppertz, Marija Curcic Djuric, Robert Hennze and Frank Kolbinger, Autoimmunity, Transplantation and Inflammatory Disease, Novartis Institutes for BioMedical Research, Novartis Pharma AG, Basel, SWITZERLAND, Basel, Switzerland

    Background/Purpose: Fibroblast-like synoviocytes (FLS) are targets of the pro-inflammatory IL-17 cytokines and a major source of inflammatory mediators in the inflamed synovium in rheumatoid arthritis…
  • Abstract Number: 428 • 2012 ACR/ARHP Annual Meeting

    TNFα Modulates the Expression of Circadian Clock Gene, Per2, Via D-Box Motif in the Promoter Region in Rheumatoid Synovial Cells

    Kohsuke Yoshida1, Akira Hashiramoto2, Takaichi Okano3, Nao Shibanuma4 and Shunichi Shiozawa5, 1Hyogo Prefectural Rehabilitation Center at Nishi-harima, Tatsuno, Japan, 2Department of Internal Medicine, Kobe University Graduate School of Medicine / The Center for Rheumatic Diseases, Kobe University Hospital, Kobe, Japan, 3The Center for Rheumatic Diseases,, Kobe University Hospital, Kobe, Japan, 4The Center for Rheumatic Diseases, Kobe University Hospital / Departmant of Orthopaedic Surgery, Kobe Kaisei Hospital, Kobe, Japan, 5Department of Medicine, Kyushu University Beppu Hospital, Beppu, Japan

    Background/Purpose: The mammalian clock genes including Clock (circadian locomotor output cycles kaput), Bmal1 (brain and muscle Arnt-like protein 1), Per (Period) and Cry (Cryptochrome) regulate…
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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.).

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