ACR Meeting Abstracts

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Abstracts tagged "IL-23"

  • Abstract Number: 1576 • 2017 ACR/ARHP Annual Meeting

    IL-23 Promotes Fecal Microbiota Dysbiosis Associated with Susceptibility to Spondyloarthritis and Ileitis in ZAP-70 Mutant SKG Mice

    Linda Rehaume1, Nicholas Matigian1, Kate Ormerod2, Alicia Kang1, Richard Linedale1, Olga Zbarskaya1, Kristine Kikly3, Joshua Daly2, Nancy Lachner2, Philip Hugenholtz2, Mark Morrison1, Kim-Anh Lê Cao4 and Ranjeny Thomas1, 1The University of Queensland Diamantina Institute, Translational Research Institute, Brisbane, Australia, 2Australian Centre for Ecogenomics, The University of Queensland, Brisbane, Australia, 3Biotechnology Discovery Research, Eli Lilly and Co, Indianapolis, IN, 4School of Mathematics and Statistics, Centre for Systems Genomics, The University of Melbourne, Melbourne, Australia

    Background/Purpose: Identification of disease-associated or protective bacteria may elucidate new biomarkers or probiotic supplements for people suffering from SpA, or for people at-risk of disease…
  • Abstract Number: 1578 • 2017 ACR/ARHP Annual Meeting

    The Initiation, but Not the Persistence, of Experimental Spondyloarthritis in HLA-B27/Huβ2m Transgenic Rats Is Crucially Dependent on the IL-23 Axis

    Melissa van Tok1,2, Songqing Na3, Joel Taurog4, Dominique Baeten2,5 and Leonie van Duivenvoorde1,2, 1Amsterdam Rheumatology and immunology Center, Academic Medical Center/University of Amsterdam, Amsterdam, Netherlands, 2Clinical Immunology and Rheumatology/Experimental immunology, Academic Medical Center/University of Amsterdam, Amsterdam, Netherlands, 3Eli Lilly and Company, Indianapolis, IN, 4Dept Int Med-Rheum Dis Div, University of Texas Southwestern Medical Center, Dallas, TX, 5Clinical Immunology and Rheumatology, Amsterdam Rheumatology and immunology Center, Academic Medical Center/University of Amsterdam, Amsterdam, Netherlands

    Background/Purpose: IL-17A is a central driver of spondyloarthritis (SpA) pathology. IL-17A production was originally proposed to be IL-23 dependent. Emerging preclinical and clinical evidence from…
  • Abstract Number: 1581 • 2017 ACR/ARHP Annual Meeting

    Differential Involvement of Synovial and Entheseal Inflammation in Mediating Pathological IL23 Axis Signaling in Spondyloarthritis

    Ed Purdue1, Josselyn Galdamez1, Madeline Epsten2, Rima Abhyankar3, Kathleen Hoyt4, Michelle Lewis4, Devan Dove4, Jon Hill5, Alexander Klimowicz4, Gerald Nabozny6, Joseph Wahle4 and Lisa A. Mandl7, 1Research, Hospital for Special Surgery, New York, NY, 2Rheumatology, Hospital for Special Surgery, New York, NY, 3Hospital for Special Surgery, New York, NY, 4Department of Immunology and respiratory discovery research, Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, CT, 5Department of Discovery research, Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, CT, 6[email protected], Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, CT, 7Rheumatology, Hospital for Special Surgery/Weill Cornell Medicine, New York, NY

    Background/Purpose: Although accumulating evidence continues to point toward a critical role for IL23 signaling in spondyloarthritis (SpA), the cellular and molecular events involved, as well…
  • Abstract Number: 11L • 2016 ACR/ARHP Annual Meeting

    BMS-986165 Is a Highly Potent and Selective Allosteric Inhibitor of Tyk2, Blocks IL-12, IL-23 and Type I Interferon Signaling and Provides for Robust Efficacy in Preclinical Models of Systemic Lupus Erythematosus and Inflammatory Bowel Disease

    Kathleen Gillooly1, Yifan Zhang1, Xiaoxia Yang1, Adriana Zupa-Fernandez1, Lihong Cheng1, Joann Strnad1, Mark Cunningham2, Elizabeth Heimrich1, Xiadi Zhou1, Jing Chen3, Charu Chaudhry3, Sha Li3, Kim McIntyre1, Julie Carman4, Ryan Moslin5, Stephen Wrobleski5, David Weinstein5 and James Burke1, 1Immunosciences Discovery Biology, Bristol-Myers Squibb, Princeton, NJ, 2Bristol-Myers Squibb, Princeton, NJ, 3Leads Discovery & Optimization, Bristol-Myers Squibb, Princeton, NJ, 4Discovery Translational Sciences Group, Bristol-Myers Squibb, Princeton, NJ, 5Immunosciences Discovery Chemistry, Bristol-Myers Squibb, Princeton, NJ

    Background/Purpose: Tyk2 mediates signaling downstream of the receptors for IL-12, IL-23 and Type I interferons, all key drivers of autoimmune disorders such as SLE. BMS-986165,…
  • Abstract Number: 960 • 2016 ACR/ARHP Annual Meeting

    Ultrasonographic Improvement of Peripheral Subclinical Enthesopathy in Therapy-Naive Patients Treated with Ustekinumab for Chronic Plaque Psoriasis: A 52-Week, Prospective, Open Label, Controlled Cohort Study

    Laura Savage1, Mark Goodfield2, Elizabeth M.A. Hensor3, Paul Emery3 and Dennis McGonagle4, 1NIHR Musculoskeletal Biomedical Research Unit, University of Leeds, Leeds, United Kingdom, 2Department of Dermatology, Leeds Centre for Dermatology, Leeds Teaching Hospitals NHS Trust, Leeds, United Kingdom, 3NIHR-Leeds Musculoskeletal Biomedical Research Unit, Leeds, United Kingdom, 4Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, United Kingdom

    Background/Purpose: Subclinical enthesopathy is recognised in up to 50% of psoriasis patients and is thought to precede inflammatory PsA. It is not known if effective…
  • Abstract Number: 1678 • 2016 ACR/ARHP Annual Meeting

    JAK STAT Kinase Cascade Regulates the IL-23/IL-17 Cytokine Axis in Psoriatic Arthritis

    Siba P. Raychaudhuri1 and Smriti K. Raychaudhuri2, 1Davis, CA, 2Rheumatology/Immunology, VA Sacramento Medical Center, Davis, CA

    Background/Purpose: Aberrant activation of IL-23/IL-17 cytokine axis is a dominant pathology in the psoriatic disease. IL-23 regulates expansion/maintenance/functional maturation of Th17 cells. Th17 cells along…
  • Abstract Number: 1752 • 2016 ACR/ARHP Annual Meeting

    IL-23 Promotes the Generation of DNT Cells and Shifts the Balance Between IL-2 and IL-17 Production in Murine and Human SLE

    Hong Dai1,2, Fan He1,2, George C. Tsokos1,2 and Vasileios C. Kyttaris1,2, 1Rheumatology, Beth Israel Deaconess Medical Center, Boston, MA, 2Harvard Medical School, Boston, MA

    Background/Purpose: MRL/lpr mice develop a chronic inflammatory disease characterized by accumulation of CD4-CD8-B220+T cells mimicking human lupus; IL-23 driven IL-17 producing cell contribute to lupus…
  • Abstract Number: 2694 • 2016 ACR/ARHP Annual Meeting

    Treatment of ZAP-70 Mutant SKG Mice with Anti-IL-23 Antibody Alters Fecal Microbiota Composition and Prevents Outgrowth of Bacteria Associated with Susceptibility to Spondyloarthritis and Ileitis

    Linda Rehaume1, Nicholas Matigian1, Alicia Kang1, Olga Zbarskaya1, Kristine Kikly2, Nancy Lachner3, Joshua Daly3, Philip Hugenholtz3, Mark Morrison1, Kim-Anh Lê Cao4 and Ranjeny Thomas1, 1Translational Research Institute, The University of Queensland Diamantina Institute, Brisbane, Australia, 2Biotechnology Discovery Research, Eli Lilly and Co, Indianapolis, IN, 3The University of Queensland, Australian Centre for Ecogenomics, Brisbane, Australia, 4Translational Research Instiute, The University of Queensland Diamantina Institute, Brisbane, Australia

    Background/Purpose: Identification of disease-associated or protective bacteria may elucidate new biomarkers or probiotic supplements for people suffering from spondyloarthritis (SpA), or for people at-risk of…
  • Abstract Number: 2711 • 2016 ACR/ARHP Annual Meeting

    Tissue-Resident IL-23 Responsive Innate T Cells in Mice Comprise Tcrαβ+ and TCRγδ+ Subsets with Overlapping Function

    Katia Urso, Imtiyaz Hossain and Joerg Ermann, Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA

    Background/Purpose: Multiple lines of evidence suggest a critical role for the IL-23/IL-17A axis in spondyloarthritis. In susceptible inbred strains, hydrodynamic injection of IL-23 minicircles into…
  • Abstract Number: 2715 • 2016 ACR/ARHP Annual Meeting

    Genetic Variants in TNF, TNFRSF1A, and IL23R Are Associated with Risk of Ankylosing Spondylitis

    Jacob Sode1,2,3, Ulla Vogel4, Steffen Bank5, Paal Skytt Andersen6, Merete Lund Hetland7, Henning Locht2, Niels H. H. Heegaard8 and Vibeke Andersen9, 1Department of Autoimmunology and Biomarkers, Statens Serum Institut, Copenhagen, Denmark, 2Department of Rheumatology, Frederiksberg Hospital, Frederiksberg, Denmark, 3Department of Rheumatology, Skåne University Hospital, Lund, Sweden, 4National Research Centre for the Working Environment, Copenhagen, Denmark, 5Institute of Human Genetics, University of Aarhus, Aarhus, Denmark, 6Microbiology & Infection Control, Statens Serum Institut, Copenhagen S, Denmark, 7DANBIO Registry and Departments of Rheumatology, Rigshospitalet (Glostrup and Blegdamsvej), University of Copenhagen, Glostrup, Denmark, 8Department of Autoimmunology & Biomarkers, Statens Serum Institut, Copenhagen, Denmark, 9Odense University Hospital, OPEN (Odense Patient data Explorative Network), Odense, Denmark

    Background/Purpose: The objective of this study was to evaluate single nucleotide polymorphisms (SNPs) involved in TNFα signaling, NF-κB activation, interferon-γ signaling, or pattern recognition receptor…
  • Abstract Number: 2830 • 2015 ACR/ARHP Annual Meeting

    Synovial Fluid T Cells of Patients with Reactive Arthritis  and Undifferentiated Spondyloarthropathy Respond to Salmonella Typhimurium Outer Membrane Protein a and  Induces IL17 and IL23 Production By  Synovial Fluid Mononuclear Cells

    Ramnath Misra1, Smriti Chaurasia1, Ajit K Shashny2 and Amita Aggarwal3,4, 1Clinical Immunology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India, 2Central Institute of Medicinal and Aromatic Plants, Scientist, Lucknow, India, 3Clinical Immunology, Additional Professor Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Lucknow, India, 4Department of Clinical Immunology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

    Background/Purpose: We have previously shown that synovial fluid mononuclear cells (SFMCs) of patients with Reactive arthritis (ReA) and undifferentiated Spondyloarthropathy (uSpA) proliferated to low molecular…
  • Abstract Number: 2838 • 2015 ACR/ARHP Annual Meeting

    Evidence of Serological IL-23/IL-17 Axis Activation in Ankylosing Spondylitis Patients with Long-Term TNF Blockade: The Missing Therapy Target?

    Fernanda M. Milanez1, Carla G.S. Saad1, Vilma S. T. Viana1, Julio C. B. Moraes1, Grégory V. Périco2, Celio R. Gonçalves1 and Eloisa Bonfá1, 1Rheumatology Division, Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil, 2Unidade Radiologica Criciuma, Criciuma, Brazil

    Background/Purpose: Spondyloarthritis (Spa) is a group of inflammatory diseases in which ankylosing spondylitis (AS) is the prototype. Despite recent advances in pathophysiology and treatment, this…
  • Abstract Number: 3056 • 2015 ACR/ARHP Annual Meeting

    Increased Circulating Th17 Cells, Serum IL-17 and Serum IL-23 in Takayasu’s Arteritis

    Ramnath Misra, Durga Prasanna Misra and Smriti Chaurasia, Clinical Immunology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

    Background/Purpose: The immune mechanisms underlying Takayasu’s arteritis (TA) are not clear. Expanded Th17 T cell subset has been demonstrated in Giant Cell Arteritis. Gamma delta…
  • Abstract Number: 199 • 2015 ACR/ARHP Annual Meeting

    Human Type 1 and Ncr-Negative Type 3 Innate Lymphoid Cells Accumulate in the Inflamed Synovium in Spondyloarthritis

    Nataliya Yeremenko1,2,3, Silvia Menegatti4, Troy Noordenbos1,2,3, Leonieke J.J. van Mens1,2, Iris C. Blijdorp1,2,3, Kristine Germar1,2,3, Jochem Bernink5, Lars Rogge4, Hergen Spits5 and Dominique Baeten1,2,3, 1Amsterdam Rheumatology and immunology Center, Amsterdam, Netherlands, 2Department of Clinical Immunology and Rheumatology, Academic Medical Centre/University of Amsterdam, Amsterdam, Netherlands, 3Laboratory of Experimental Immunology, Academic Medical Center/University of Amsterdam, Amsterdam, Netherlands, 4Immunoregulation Unit, Institut Pasteur, Paris, France, 5Department of Cell Biology and Histology, Academic Medical Centre/University of Amsterdam, Amsterdam, Netherlands

    Background/Purpose:  Spondyloarthritis (SpA) is a major form of chronic inflammatory arthritis characterized by inflammation of axial and peripheral joints and by pathologic new bone formation…
  • Abstract Number: 2144 • 2015 ACR/ARHP Annual Meeting

    Efficacy and Safety of Different Dose Regimens of a Selective IL-23p19 Inhibitor (BI 655066) Compared with Ustekinumab in Patients with Moderate-to-Severe Plaque Psoriasis with and without Psoriatic Arthritis

    Kim Papp1, Alan Menter2, Howard Sofen3, Stephen Tyring4, Jean-Philippe Lacour5, Beate Berner6, Nathan Bennett7, Stella Aslanyan7, Mary Flack7 and Paul Scholl7, 1Probity Clinical Research, Waterloo, ON, Canada, 2Baylor Research Institute, Dallas, TX, 3Dermatology Research Associates, Los Angeles, CA, 4Center for Clinical Studies, Houston, TX, 5Dermatology Department, Hôpital de L’Archet, Nice, France, 6Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach, Germany, 7Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, CT

     Background/Purpose: IL-23 is essential for the differentiation and maintenance of Th17 cells in psoriasis and psoriatic arthritis (PsA). We assessed the efficacy and safety of…
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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.).

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].

ACR Abstract Embargo Policy

Accepted abstracts are made available to the public online in advance of the meeting and are published in a special online supplement of Arthritis & Rheumatology. Information contained in those abstracts may not be released until the abstracts appear online. 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 a scientific presentation or presentation of additional new information that will be available at the time of the meeting) is under embargo until Saturday, November 11, 2023.

Violation of this policy may result in the abstract being withdrawn from the meeting and other measures deemed appropriate. Authors are responsible for notifying financial and other sponsors about this policy. If you have questions about the abstract embargo policy, please contact the public relations department at [email protected].

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