Abstracts tagged "Apoptosis"

Abstract Number: 1835 • 2017 ACR/ARHP Annual Meeting
Microglial Defects Contribute to Neuropsychiatric Symptoms of Systemic Lupus Erythematosus
Hadijat Makinde¹, Philip J. Homan², Harris Perlman² and Carla Cuda², ¹Northwestern University, Chicago, IL, ²Department of Medicine Division of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL
Background/Purpose: Neuropsychiatric symptoms of systemic lupus erythematosus (NP-SLE), including headaches, cognitive dysfunction and psychiatric disorders, appear in up to 75% of SLE patients and may…
Abstract Number: 2576 • 2017 ACR/ARHP Annual Meeting
Caspase 8 in Dendritic Cells Suppresses IRF5 Activation through Endosomal TLR Signaling to Prevent SLE-like Disease
FuNien Tsai¹, Harris Perlman² and Carla Cuda², ¹Medicine-Rheumatology, Northwestern University-Feinberg School of Medicine, Chicago, IL, ²Department of Medicine Division of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL
Background/Purpose: Previous studies implicate dendritic cells (DCs) in the pathogenesis of systemic lupus erythematosus (SLE), yet the mechanisms underlying this involvement are not yet clear.…
Abstract Number: 810 • 2016 ACR/ARHP Annual Meeting
Microrna-125b As a Potential Anti-Fibrotic and Anti-Apoptotic Regulator in Systemic Sclerosis
Anastasiia Kozlova¹, Elena Pachera¹, Florian Renoux², Michal Rudnik¹, Britta Maurer¹, Astrid Jüngel³, Joerg H.W Distler⁴, Gabriela Kania¹ and Oliver Distler¹, ¹Department of Rheumatology, University Hospital Zurich, Zurich, Switzerland, ²Depertment of Rheumatology, University Hospital Zurich, Schlieren, Switzerland, ³Ctr Exp Rheum, Univ Hosp Zurich / Zurich Ctr Integr Hum Physiol (ZIHP), Zurich, Switzerland, ⁴Department of Internal Medicine 3, Rheumatology and Immunology, Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany
Background/Purpose: MicroRNAs (miRs) are a class of small, noncoding RNAs that regulate many biological processes. Some microRNAs are involved in skin fibrosis. Here, we aimed…
Abstract Number: 1747 • 2016 ACR/ARHP Annual Meeting
Dissecting the Role of Single Complement Deficiencies in a Novel Model for Apoptotic Cell-Induced Lupus
Lucrezia Colonna¹, Clayton J. Sontheimer², Lena M. Tanaka³, Kelly L. Hudkins⁴, Charles E. Alpers⁴, Keith B. Elkon¹ and YuFeng Peng³, ¹Department of Medicine, Division of Rheumatology, University of Washington, Seattle, WA, ²Pediatric Rheumatology, University of Washington, Seattle, WA, ³Division of Rheumatology, University of Washington, Seattle, WA, ⁴Pathology, University of Washington, Seattle, WA
Background/Purpose: The role of complement in Systemic Lupus Erythematosus (SLE) is complex as complement deficiencies in early components of the classical pathway cause lupus with…
Abstract Number: 1916 • 2016 ACR/ARHP Annual Meeting
Heightened MAIT Cell Sensitivity to MR1 Ligands Could Impact Control of Dysbiosis in Patients with Rheumatoid Arthritis and Ankylosing Spondylitis
Diahann Jansen¹, Elizabeth Klinken¹, Hendrik Nel², Soi Cheng Law², Helen Benham^3,4,5, Lisa Cummins⁶, Matthew Brown⁷, Tony Kenna², Ligong Liu⁸, David Fairlie⁸, Jamie Rossjohn^9,10,11, Mark Morrison³, Ranjeny Thomas³, Paraic O Cuiv¹, James McCluskey¹² and Alexandra Corbett¹², ¹The University of Queensland Diamantina Institute, Translational Research Institute, Woolloongabba, Australia, ²The University of Queensland Diamantina Institute, Translational Research Institute, Brisbane, Australia, ³Translational Research Institute, The University of Queensland Diamantina Institute, Woolloongabba, Australia, ⁴University of Queensland School of Medicine, Brisbane, Australia, ⁵Rheumatology, Princess Alexandra Hospital, Woolloongabba, Australia, ⁶Princess Alexandra Hospital, Woolloongabba, Australia, ⁷Queensland University of Technology, Brisbane, Australia, ⁸Institute for Molecular Bioscience, University of Queensland, Brisbane, Australia, ⁹Infection and Immunity Program, Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology, Monash University, Clayton, Australia, ¹⁰Institute of Infection and Immunity, Cardiff University School of Medicine, Cardiff, United Kingdom, ¹¹Australian Research Council Centre of Excellence in Advanced Molecular Imaging, Monash University, Clayton, Australia, ¹²Department of Microbiology & Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Australia
Background/Purpose: Mucosal associated invariant T (MAIT) cells are an innate-like lymphocyte population predominant at mucosal sites, which express a semi-invariant T cell receptor restricted to…
Abstract Number: 2060 • 2016 ACR/ARHP Annual Meeting
Bim Suppresses the Development of SLE By Limiting Macrophage Inflammatory Responses
FuNien Tsai¹, Carla Cuda², Harris R. Perlman³, Philip J. Homan⁴, Salina Dominguez², Alexander Shaffer³, George Kenneth Haines III⁵ and Jack Hutcheson⁶, ¹Medicine-Rheumatology, Northwestern University-Feinberg School of Medicine, Chicago, IL, ²Northwestern University, Chicago, IL, ³Department of Medicine, Division of Rheumatology, Northwestern University Feinberg School of Medicine, Northwestern University, Chicago, IL, ⁴Medicine-Rheumatology, Northwestern University, Chicago, IL, ⁵Mount Sinai, New York, NY, ⁶UT Southwestern, Dallas, TX
Background/Purpose: The Bcl-2 family guards the mitochondrial apoptotic pathway. Among numerous Bcl-2 antagonists, only the loss of Bim in mice leads to the development of…
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: 2558 • 2016 ACR/ARHP Annual Meeting
Dissociation of the Inhibitory Apoptosis Stimulating Protein of p53 (iASPP) Binding with Transcription Factor p73 Induces Synovial Fibroblast Apoptosis in the Rheumatoid Joint
Chrong-Reen Wang¹, Shih-Yao Chen¹, Ai-Li Shiau², Ming-Fei Liu¹ and Chao-Liang Wu³, ¹Internal Medicine, National Cheng Kung University Medical College and Hospital, Tainan, Taiwan, ²Microbiology and Immunology, National Cheng Kung University Medical College, Tainan, Taiwan, ³Biochemistry and Molecular Biology, National Cheng Kung University Medical College, Tainan, Taiwan
Background/Purpose: Apoptosis-resistant synovial fibroblasts (SFs) constitute the major cell component of pannus tissues in rheumatoid arthritis (RA). In tumor cells, the binding of inhibitory…
Abstract Number: 2561 • 2016 ACR/ARHP Annual Meeting
A Novel Pharmacological Action of MTX on RA Fibroblast-like Synoviocytes Via Circadian Clock Genes
Kohjin Suzuki¹, Kohsuke Yoshida¹, Teppei Hashimoto², Kenta Kaneshiro¹, Ayako Nakai¹, Naonori Hashimoto¹, Yoshiko Kawasaki², Nao Shibanuma³, Natsuko Nakagawa⁴, Yoshitada Sakai⁵ and Akira Hashiramoto⁶, ¹Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan, ²Department of Rheumatology, Kobe Kaisei Hospital, Kobe, Japan, ³Departmant of Orthopaedic Surgery, Kobe Kaisei Hospital, Kobe, Japan, ⁴Department of Orthopaedic Surgery, Konan-Kakogawa Hospital, Kakogawa, Japan, ⁵Division of Rehabilitation Medicine, Kobe University Graduate School of Medicine, Kobe, Japan, ⁶Department of Biophysics, Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan
Background/Purpose: The circadian rhythm is disrupted in patients with rheumatoid arthritis (RA), and we have shown that tumor necrosis factor(TNF)-ƒ¿ inhibits the expression of circadian…
Abstract Number: 3143 • 2016 ACR/ARHP Annual Meeting
The Caspase 8/RIPK3 Signaling Axis in Dendritic Cells Controls Joint Homeostasis Under Steady-State and Arthritic Conditions
Salina Dominguez¹, Harris R. Perlman² and Carla Cuda¹, ¹Northwestern University, Chicago, IL, ²Department of Medicine, Division of Rheumatology, Northwestern University Feinberg School of Medicine, Northwestern University, Chicago, IL
Background/Purpose: Rheumatoid arthritis (RA) manifests in persistent synovial inflammation, cellular infiltration and pro-inflammatory cytokine production, and results in progressive joint destruction. Dendritic cells (DCs) have…
Abstract Number: 3215 • 2015 ACR/ARHP Annual Meeting
Bim Suppresses the Development of SLE By Limiting Macrophage Inflammatory Responses
Fu-Nien Tsai¹ and Harris R. Perlman², ¹Medicine, Rhuematology, Northwestern University, Chicago, IL, ²Feinberg School of Medicine, Northwestern University, Chicago, IL
Background/Purpose: The Bcl-2 family guards the mitochondrial apoptotic pathway. Among numerous Bcl-2 antagonists, only the loss of Bim in mice leads to the development of…
Abstract Number: 8 • 2015 ACR/ARHP Annual Meeting
Bay 11-7085 Induces Glucocorticoid Receptor Activation and Autophagy to Initiate Human Synovial Fibroblast Cell Death
Biserka Relic¹, Edith Charlier², Céline Deroyer¹, Olivier Malaise¹, Sophie Neuville¹, Aline Desoroux¹, Philippe Gillet³, Michel G. Malaise¹ and Dominique de Seny¹, ¹Department of Rheumatology- GIGA Research - Arthropôle - University of Liège - CHU Liège, Liège, Belgium, ²Department of Rheumatology, Department of Rheumatology- GIGA Research - Arthropôle - University of Liège - CHU Liège, Liège, Belgium, ³Orthopaedic Surgery Department-University of Liège-CHU de Liège, Liège, Belgium
Background/Purpose: BAY 11-7085 is an inhibitor of IκBα phosphorylation that leads to NF-κB inactivation and downregulation of inflammation in mouse model of asthma, in articular…
Abstract Number: 810 • 2015 ACR/ARHP Annual Meeting
Human Parvovirus B19 Nonstructural Protein 1 (NS1) Helicase Breaks Tolerance to Self dsDNA: A Model for Viral Induction of Autoimmunity
Heidi Pirttinen¹, Kanoktip Puttaraksa¹, Robert J. Lagier², Stanley J. Naides³ and Leona Gilbert¹, ¹Department of Biological and Environmental Science, University of Jyväskylä, Jyväskylä, Finland, ²Research Support, Alameda, Quest Diagnostics Alameda, Alameda, CA, ³Immunology, Quest Diagnostics Nichols Institute, San Juan Capistrano, CA
Background/Purpose: B19 virus (B19V) is common, infects all ages, and is associated with various clinical syndromes including SLE-like autoimmunity. We previously demonstrated that B19 NS1,…
Abstract Number: 1037 • 2015 ACR/ARHP Annual Meeting
Impaired Regulatory T Cell Survival in the Pathogenesis of Autoreactive Arthritis Mediated By CD11c-Deletion of Flip
Qi Quan Huang¹, Renee E. Doyle¹, Robert Birkett², Deyu Fang³, Syamal K. Datta¹ and Richard M. Pope¹, ¹Medicine/Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL, ²Division of Rheumatology, Department od Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, ³Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL
Background/Purpose: We have generated a mouse line with Flip conditionally deleted in CD11c-cre expressing cells (CD11c-Flip-KO, named HUPO), which spontaneously develops erosive arthritis resembling rheumatoid…
Abstract Number: 1616 • 2015 ACR/ARHP Annual Meeting
Identification of Genes Regulating TRAIL-Induced Apoptosis in Rheumatoid Arthritis Fibroblasts-like Synoviocytes (RA FLS)
Rachel Audo^1,2, Bernard Combe^3,4, Michael Hahne⁵ and Jacques Morel⁶, ¹Rheumatology, Teaching Hospital of Lapeyronie, Montpellier, France, ²IGMM, CNRS UMR5535, Montpellier, Montpellier, France, ³Department of Rheumatology, Lapeyronie Hospital, Montpellier, France, ⁴Montpellier University, Montpellier, France, ⁵IGMM-CNRS UMR5535, Montpellier, France, ⁶Department of rheumatology, Lapeyronie Hospital and Montpellier University, Montpellier, France
Background/Purpose: We previously described that sensitivity to TRAIL-induced apoptosis varied in rheumatoid arthritis (RA) fibroblasts-like-synoviocytes (FLS) from one patient to another, and was inversly correlated…

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