Abstracts tagged "Animal Model"

Abstract Number: 0785 • ACR Convergence 2024
Exploring the Link Between Atgl-Dependent Lipolysis and Dermal Fibrosis in Systemic Sclerosis
Elizabeth Caves¹, Agrani Dixit¹, Anna Jussila², Vivian Lei³, Hailey Edelman⁴, Muhammad Hamdan⁵, Ian Odell⁵, Monique Hinchcliff⁶, Radhika Atit⁷ and Valerie Horsley¹, ¹Yale School of Medicine, New Haven, CT, ²Stanford Medicine, Stanford, CA, ³University of North Carolina School of Medicine, Chapel Hill, ⁴Vanderbilt School of Engineering, New Haven, ⁵Yale School of Medicine, New Haven, ⁶Yale School of Medicine, Westport, CT, ⁷Case Western Reserve University College of Arts and Sciences, Cleveland
Background/Purpose: Resident lipid-filled dermal adipocytes are depleted in both systemic sclerosis (SSc) and scleroderma mouse models, but mechanisms are poorly understood. We undertook studies in mouse…
Abstract Number: 1838 • ACR Convergence 2024
M5542: A Potent CD80, CD86, and OX40L Antagonist Fusion Molecule for the Treatment of Autoimmune Diseases
Michelle Downing¹, Ling Zhang¹, Aditee Desphpande¹, Hong Zhang¹, Ohad Tarcic², Mira toister-achituv², Alec Gross³, Gang Chen³ and Chia Chi Sun¹, ¹EMD Serono Research and Development Institute, Inc., Billerica, MA, ²Inter-lab Ltd, Merck KGaA, Yavne, Israel, ³EMD Serono Reserch and Development Institute, Inc, Billerica, MA
Background/Purpose: Overactive adaptive immune responses contribute to many autoimmune diseases such as systemic lupus erythematosus (SLE). Chronically activated autoreactive T-effector cells play a pivotal role…
Abstract Number: 0830 • ACR Convergence 2024
Activation of Autoreactive Lymphocytes in the Lung by STING Gain-of-function Mutation Expressing Radioresistant Cells
Kevin Gao¹, Kristy Chiang¹, Sharon Subramanian¹, Xihui Yin², Paul Utz³, Kerstin Nundel¹, Katherine A. Fitzgerald⁴ and Ann Marshak-Rothstein¹, ¹UMass Chan Medical School, Worcester, MA, ²Stanford University School of Medicine, Palo Alto, CA, ³Stanford University, Stanford, CA, ⁴UMass Chan Medical School, Worchester, MA
Background/Purpose: Gain-of-function mutations in STING, a critical mediator of dsDNA sensing, lead to a severe autoinflammatory syndrome known as STING-Associated Vasculopathy with onset in Infancy…
Abstract Number: 1853 • ACR Convergence 2024
Mutated Nod2 Enhances Pathogenic Th17 Responses That Promote Experimental Blau Syndrome
Leah Huey¹, Emily Vance¹, Kofi Asare-Konadu² and Ruth Napier³, ¹Oregon Health & Science University, Portland, OR, ²Department of Molecular Microbiology and Immunology, Oregon Health & Science University, Portland, OR, ³Department of Molecular Microbiology and Immunology and Division of Arthritis and Rheumatic Disease, Oregon Health & Science University, VA Portland Health Care System, Portland, OR
Background/Purpose: Blau syndrome, a pediatric rheumatological disease characterized by uveitis, arthritis, and dermatitis, is caused by a single point mutation in the gene NOD2. Nod2…
Abstract Number: 0023 • ACR Convergence 2024
Adenosine and Guanosine-based Oligonucleotide Attenuates Catabolic Phenotypes in Chondrocytes and Slows Progression of Surgically Induced Osteoarthritis
Yoonhee Kim¹, Jin Han² and Seungwoo Han³, ¹Kyungpook National University School of Medicine, Buk-gu, Daegu, Republic of Korea, ²Kyungpook National University, Buk-gu, Daegu, Republic of Korea, ³Kyungpook national university hospital, Daegu, South Korea
Background/Purpose: Adenosine is a potent endogenous modulator of inflammation; however, its clinical application is limited due to its extremely short half-life in blood. In this…
Abstract Number: 0922 • ACR Convergence 2024
Generation and Pathophysiological Analysis of M694I Variant Knock-in Mice of Human MEFV Gene: Insights from Single-Cell RNA Sequencing
Tomohiro Koga, Yoshika Tsuji and Atsushi Kawakami, Nagasaki University, Nagasaki, Japan
Background/Purpose: The primary objective of this study was to generate knock-in mice with the M694I variant of the human MEFV gene, a critical variant in…
Abstract Number: 1854 • ACR Convergence 2024
TCR-Nck Modulators: Pioneering Oral Modulation of T Cell Receptor Activation Holding the Promise of Treating Autoimmune Diseases
Christopher VanDeusen¹, Shannon Dwyer², Aldo Borroto³, Andres Gagete¹, D Scott Batty Jr¹ and Balbino Alarcon³, ¹Artax Biopharma, Inc, Cambridge, MA, ²Artax Biopharma, Inc., Cambridge, ³Centro de Biología Molecular Severo Ochoa, Madrid, Spain
Background/Purpose: Loss of T-cell tolerance to self-antigens underlies the development of all autoimmune diseases, and despite progress, there remains a significant unmet need for patients.…
Abstract Number: 0031 • ACR Convergence 2024
Beyond Pain and Inflammation: Intra-articular Liraglutide’s Comprehensive Benefits on Synovial Health and Cartilage in Osteoarthritis Compared to Dexamethasone
Coralie Meurot¹, Celine Martin¹, Margot Vieubled¹, Jerome Breton¹, Indira Toillon², Revital Rattenbach³ and Francis Berenbaum², ¹4Moving Biotech, lille, France, ²Sorbonne University, Paris, France, ³4Moving Biotech, Paris, France
Background/Purpose: Osteoarthritis (OA) is an age-related joint disease that causes chronic pain and limited mobility. Patients mainly have access to therapies aimed at reducing inflammation…
Abstract Number: 0923 • ACR Convergence 2024
Immunization of Arthritis Prone Mice with Malondialdehyde-Acetaldehyde Modified Vimentin Induces Post-Translational Protein Modifications and Extracellular Matrix Deposition in Heart Tissues
Kimberley Sinanan¹, Wenxian Zhou², Michael Duryee¹, Nozima Aripova¹, Jill Poole¹, Carlos Hunter¹, Amy Nelson¹, Tate Johnson¹, Daniel Anderson³, Ted Mikuls¹ and Geoffrey Thiele¹, ¹University of Nebraska Medical Center, Omaha, NE, ²University of Nebraska Medical Center, Bellevue, NE, ³University of Nebraska Medical Center, Durham, NC
Background/Purpose: Recent studies have highlighted the importance of malondialdehyde-acetaldehyde (MAA)-modified proteins and resulting immune responses in the pathogenesis of rheumatoid arthritis (RA). MAA adducts have…
Abstract Number: 2078 • ACR Convergence 2024
Increased RAGE Expression in Myositis
Madison King¹, Rita Spathis², Elizabeth Bagley¹ and Melissa Morales³, ¹Binghamton University, Johnson City, NY, ²Binghamton University School of Pharmacy and Pharmaceutical Sciences, Johnson City, NY, ³SUNY Binghamton, Johnson City, NY
Background/Purpose: Myositis is a broad term for a group of rare autoimmune diseases that cause persistent muscle inflammation, weakness, and fatigue. Currently, first-line treatment for…
Abstract Number: 0032 • ACR Convergence 2024
Increased Expression of Malondialdehyde-Acetaldehyde and Citrullinated Proteins in Myocardial Tissues During the Early Evolution of Collagen-Induced Arthritis
Wenxian Zhou¹, Michael Duryee², Nozima Aripova², Jill Poole², Carlos Hunter², Amy Nelson², Tate Johnson², Daniel Anderson³, Geoffrey Thiele² and Ted Mikuls², ¹University of Nebraska Medical Center, Bellevue, NE, ²University of Nebraska Medical Center, Omaha, NE, ³University of Nebraska Medical Center, Durham, NC
Background/Purpose: The risk of heart failure (HF) is increased in patients with rheumatoid arthritis (RA), although mechanisms of myocardial dysfunction underlying HF development in RA…
Abstract Number: 0924 • ACR Convergence 2024
The Cytosolic DNA Sensor AIM2 Regulates Bone Homeostasis Through Bone Progenitor Cell Differentiation
Jia (Sijia) Chen¹, Yukiko Maeda², Catherine Manning³, Victor Le⁴, Jae-Hyuck Shim⁵, Katherine A. Fitzgerald⁶ and Ellen Gravallese⁷, ¹Brigham and Women's Hospital, Boston, MA, ²Sanofi, worcester, MA, ³Brigham and Women's Hospital, Dedham, MA, ⁴Digital Biology, Boston, MA, ⁵University of Massachusetts, Worcester, MA, ⁶UMass Chan Medical School, Worchester, MA, ⁷Brigham and Women's Hospital, Harvard Medical School, Chestnut Hill, MA
Background/Purpose: Innate sensing pathways and inflammasomes play an important role in autoimmunity and aging. AIM2 is a DNA sensor that triggers inflammasome assembly in myeloid…
Abstract Number: 2539 • ACR Convergence 2024
Telocytes Integrated into Mast Cells and Joint-Draining Lymphatic Vessels Potentially Regulate Lymphatic Clearance
Yue Peng¹, H. Mark Kenney², Karen Bentley¹, Lianping Xing³, Benjamin Korman⁴, Christopher Ritchlin⁵ and Edward Schwarz¹, ¹University of Rochester School of Medicine and Dentistry, Rochester, NY, ²University of Rochester School of Medicine and Dentistry, Henrietta, NY, ³University of Rochester School of Medicine and Dentistry, Webster, NY, ⁴University of Rochester, Rochester, NY, ⁵Department of Medicine, Allergy, Immunology, and Rheumatology Division, University of Rochester Medical School, Canandaigua, NY
Background/Purpose: Rheumatoid arthritis (RA) patients and TNF-transgenic mice have lymphatic dysfunction (1). Recently, we showed mast cells involvement, as genetic ablation and drug inhibition decreased…
Abstract Number: 0068 • ACR Convergence 2024
Enhanced Expression of GPR65 in Inflammatory Sites and Bone Formation Regions in Ankylosing Spondylitis: Evidence from ScRNA-seq Analysis
Yong-Wook Park¹, Ki-Jeong Park², Sungsin Jo³, Tae-Hwan Kim⁴ and Tae-Jong Kim¹, ¹Department of Rheumatology, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea, ²Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea, ³Hanyang University Institute for Rheumatology Research, Seoul, Republic of Korea, ⁴Department of Rheumatology, Hanyang University Hospital for Rheumatic Diseases, Seoul, Republic of Korea
Background/Purpose: Ankylosing spondylitis (AS) is a chronic inflammatory disease primarily affecting the axial skeleton. T helper 17 (Th17) cells play a pivotal role in the…
Abstract Number: 0925 • ACR Convergence 2024
Macrophages Produce Bone Anabolic Factors in Settings of Inflammation-Induced Bone Formation
Jia (Sijia) Chen¹, Megan Hanlon², Catherine Manning³, Susan MacLauchlan¹, Paul Hoover⁴, Christian Jacome-Galarza⁵ and Ellen Gravallese⁶, ¹Brigham and Women's Hospital, Boston, MA, ²Brigham and Women’s Hospital, Boston, MA, ³Brigham and Women's Hospital, Dedham, MA, ⁴Brigham and Women's Hospital, SWAMPSCOTT, MA, ⁵Brigham and Women's Hospital, Harvard Medical School, Boston, MA, ⁶Brigham and Women's Hospital, Harvard Medical School, Chestnut Hill, MA
Background/Purpose: Understanding the pathogenesis of inflammation-induced pathologic bone formation remains a significant challenge in spondyloarthritis patients. We thought to uncover the pivotal events driving the…

1
2
3
…
12
Next Page »

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].