Abstracts tagged "innate immunity"

Abstract Number: 2577 • 2017 ACR/ARHP Annual Meeting
Segmented Filamentous Bacteria Colonization Exacerbate Lupus Nephritis in NZM2410 Mice and Causes an Expansion of Intestinal Group 3 Innate Lymphoid Cells
Giancarlo R. Valiente¹, Jeffrey Hampton², Takuma Wada³, Perry Blough³, William Willis⁴, Nicholas A. Young⁴, Lai-Chu Wu⁵ and Wael Jarjour⁶, ¹Rheumatology & Immunology, The Ohio State University Wexner Medical Center, Columbus, OH, ²Immunology and Rheumatoloty, The Ohio State University Wexner Medical Center, Columbus, OH, ³The Ohio State University, Columbus, OH, ⁴Immunology and Rheumatology, The Ohio State University Wexner Medical Center, Columbus, OH, ⁵Biological Chemistry and Pharmacology, The Ohio State University Wexner Medical Center, Columbus, OH, ⁶Department of Rheumatology/Medicine, Ohio State University, Columbus, OH
Title: Segmented Filamentous Bacteria Colonization Exacerbate Lupus Nephritis in NZM2410 Mice and Causes an Expansion of Intestinal Group 3 Innate Lymphoid Cells Background/Purpose: Innate Lymphoid…
Abstract Number: 2643 • 2017 ACR/ARHP Annual Meeting
HO-1 Expression in Monocytes Might Regulate Kidney Damage in Lupus Nephritis Patients
Loreto Cuitino^1,2, Javiera Obreque^1,2, Patricia Gajardo-Meneses^1,2, Gonzalo P. Méndez^2,3, Alexis M. Kalergis^2,4 and Carolina Llanos^1,2, ¹Departamento de Inmunología Clínica y Reumatología, Santiago, Chile, ²Escuela de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile, ³Departamento de Anatomía Patológica, Santiago, Chile, ⁴Millennium Institute on Immunology and Immunotherapy and Departamento de Endocrinología, Santiago, Chile
Background/Purpose: It is well established that up to 70% of systemic lupus erythematosus (SLE) patients will develop Lupus Nephritis (LN). Recent studies have revealed that…
Abstract Number: 2901 • 2017 ACR/ARHP Annual Meeting
Anti-Inflammatory Mechanism of Lubricin/Proteoglycan 4 (PRG4) in Monosodium Urate (MSU)-Crystal Induced Arthritis in THP-1 Macrophages Is Mediated By NALP3 Inflammasome.
Anthony M. Reginato¹, Changqi Sun², Tannin Schmidt³, Elsaid Khalid⁴ and Gregory Jay⁵, ¹Division of Rheumatology, The Warren Alpert School Of Medicine of Brown University, Providence, RI, ²Division of Rheumatology, Rhode Island Hosital/The Warren Alpert School of Medicine of Brown University, Providence, RI, ³Kinesiology and Schulich School of Engineering, University of Calgary, Calgary, AB, Canada, ⁴Department of Biomedical and Phramaceutical Science, Chapman University School of Pharmacy, Irvine, CA, ⁵Emergency Medicine and Engineering, The Warren Alpert Medical School Brown University, Providence, RI
Background/Purpose: Lubricin/proteoglycan-4 (PRG4) is a mucinous glycoprotein secreted by synovial fibroblast and superficial zone chondrocytes. PRG4 has a multifaceted homeostatic role in the joint including…
Abstract Number: 403 • 2017 ACR/ARHP Annual Meeting
Cardiac Immune Cells in SKG Mice with Inflammatory Arthritis before and after Myocardial Infarction
Christine Hsieh¹, Isabella Imhof², Luyi Li³, Erene Niemi¹, Matthew Bell¹, Joel Karliner⁴ and Mary Nakamura⁵, ¹Medicine, SFVA/UCSF, San Francisco, CA, ²Medicine, SFVA/NCIRE, San Francisco, CA, ³SFVA/UCSF, San Francisco, CA, ⁴Medicine, SFVA/UCSF, San, CA, ⁵Department of Medicine, Division of Rheumatology, UCSF/SFVA, San Francisco, CA
Background/Purpose: Cardiovascular disease is a major cause of morbidity and mortality in patients with rheumatoid arthritis (RA). RA patients have an increased incidence of both…
Abstract Number: 544 • 2017 ACR/ARHP Annual Meeting
Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of PF-06650833, a Novel, Potentially First-in-Class Inhibitor of Interleukin-1 Receptor Associated Kinase-4 (IRAK-4) in Healthy Subjects
Spencer Danto¹, Negin Shojaee¹, Cheryl Li¹, Steven A. Gilbert², Ravi Shankar Singh¹, Zorayr Manukyan¹ and Iain Kilty¹, ¹Worldwide Research and Development, Pfizer, Inc., Cambridge, MA, ²Pfizer, Inc., Cambridge, MA
Background/Purpose: IRAK‑4 is a key node in innate immune signaling and is activated by the interleukin (IL)‑1 family receptors (IL‑1R, IL‑18R, and IL‑33R), in addition…
Abstract Number: 1062 • 2017 ACR/ARHP Annual Meeting
Ptpn22 Regulates Synovial Slam Family Receptor Expression during Toll-like Receptor-Driven Suppression of Inflammatory Arthritis
David Ewart¹, Juan Abrahante Lloréns² and Erik J. Peterson³, ¹Rheumatology, University of Minnesota, Minneapolis, MN, ²Informatics Institute (UMII), University of Minnesota, Minneapolis, MN, ³Center for Immunology/Department of Medicine, University of Minnesota, Minneapolis, MN
Background/Purpose: Genetic factors contribute strongly to Rheumatoid arthritis (RA) risk. Protein tyrosine phosphatase non-receptor 22 [PTPN22] encodes the hematopoietic-specific Lymphoid Phosphatase [“Lyp”]. A PTPN22 coding…
Abstract Number: 1065 • 2017 ACR/ARHP Annual Meeting
Mucosal-Associated Invariant T Cell Deficiency in Systemic Lupus Erythematosus Is Realted to an Intrinsic Defect in the Ca2+/Calcineurin/NFAT1 Signaling Pathway
Yong-Wook Park¹, Young-Nan Cho², Hye-Mi Jin¹, Tae-Jong Kim³ and Seung-Jung Kee⁴, ¹Rheumatology, Chonnam National University Medical School and Hospital, Gwangju, Korea, Republic of (South), ²Rheumatology, Chonnam National University Hospital and Medical School, Gwangju, MN, Korea, Republic of (South), ³Chonnam Nat`l University Medical School&Hospital, Chonnam, Korea, Republic of (South), ⁴Laboratory Medicine, Chonnam National University Medical School and Hospital, Gwangju, Korea, Republic of (South)
Background/Purpose: Mucosal-associated invariant T (MAIT) cells contribute to protection against certain microorganism infections and play an important role in mucosal immunity. However, the role of…
Abstract Number: 1068 • 2017 ACR/ARHP Annual Meeting
Impact of TNF Antagonist Treatment on the Gut Microbiome In Vivo
Odile Gabay¹, Jonathan Vicenty², Grant Wunderlin³, Linda Tiffany², Wells Wu⁴, Vahan Simonyan⁵ and Kathleen A Clouse⁶, ¹Office of Biotechnology Products /Center for Drug Evaluation and Research DBRRI, U.S. Food and Drug Administration, Silver Spring, MD, ²Office of Biotechnology Products, Center for Drug Evaluation and Research, DBRRI, U.S. Food and Drug Administration, Silver Spring, MD, ³Center for Drug Evaluation and Research CDER DBRRI, U.S. Food and Drug Administration, Silver Spring, MD, ⁴Center for Biologic Evaluation and Research OMPT, U.S. Food and Drug Administration, Silver Spring, MD, ⁵Center for Biologic Evaluation and Research, U.S. Food and Drug Administration, Silver Spring, MD, ⁶Office of Biotechnology Products /Center for Drug Evaluation and Research,DBRRI, U.S. Food and Drug Administration, Silver Spring, MD
Background/Purpose: Auto-immune diseases are in constant progression in the US. Biologic therapeutics have been used successfully to treat these diseases, but have presented some unique…
Abstract Number: 1077 • 2017 ACR/ARHP Annual Meeting
The Lectin Pathway of the Complement System Is Activated in Patients with Systemic Lupus Erythematosus
Anne Troldborg^1,2, Steffen Thiel³, Marten Trendelenburg⁴, Justa Friebus-Kardash⁵, Josephine Nehring⁵, Rudi Steffensen⁶, Søren Werner Karlskov Hansen⁷, Magdalena Janina Laska¹, Bent Deleuran⁸, Jens Christian Jensenius¹, Anne Voss⁹ and Kristian Stengaard-Pedersen¹⁰, ¹Biomedicine, Aarhus University, Aarhus, Denmark, ²clinical medicine, Aarhus University, Aarhus, Denmark, ³Institute of Biomedicine, Aarhus University, Aarhus, DK, Aarhus, Denmark, ⁴Department of Biomedicine, Division of Internal Medicine, Basel, Switzerland, ⁵University Hospital Basel, Division of Internal Medicine, Basel, Switzerland, ⁶Department of Clinical Immunology, Aalborg University Hospital, Aalborg, Denmark, ⁷Department of Cancer and Inflammation Research, University of Souther Denmark, Odense, Denmark, ⁸Department of Biomedicine, Aarhus University, Aarhus, Denmark, ⁹Rheumatology, Odense University Hospital, Odense, Denmark, ¹⁰Department of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark
Background/Purpose: The pathogenesis of Systemic Lupus Erythematosus (SLE) involves complement activation. It is well established that activation of complement through the classical pathway (CP) and…
Abstract Number: 1338 • 2017 ACR/ARHP Annual Meeting
Important Role of CD11c+ Dendtritic Cells in Inflammatory Arthritis
Antonia Puchner¹, Victoria Saferding¹, Michael Bonelli², Harald Leiss³, Gerhard Krönke⁴, René Pfeifle⁵, Josef S. Smolen⁶, Kurt Redlich⁷ and Stephan Blüml⁶, ¹Medical University of Vienna, Austria, Vienna, Austria, ²Rheumatology, Medical University of Vienna, Vienna, Austria, ³Rheumatology, Medical University Vienna, Vienna, Austria, ⁴Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Department of Internal Medicine 3 – Rheumatology and Immunology, Universitätsklinikum Erlangen, Erlangen, Germany., Erlangen, Austria, ⁵Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany, ⁶Medical University Vienna, Division of Rheumatology, Department of Internal Medicine III, Vienna, Austria, ⁷Division of Rheumatology, Medical University of Vienna, Vienna, Austria
Background/Purpose: Dendritic cells (DCs) are important antigen presenting cells (APCs) and therefore they play an important role in bridging the innate and the adaptive immune…
Abstract Number: 1663 • 2017 ACR/ARHP Annual Meeting
De Novo Mutation in ΑCΑCΒ in Childhood Onset SLE Highlights a Novel Role As Modulator of Nucleic Acid Sensor-Driven Type I Interferon Responses
Isaac Harley¹, Hanna Schulz¹, John Cambier², Leah C. Kottyan³, John B. Harley⁴, V. Michael Holers⁵, Hermine I. Brunner⁶, Kristine Kuhn¹, Kevin D. Deane¹ and Kenneth Kaufman⁷, ¹Division of Rheumatology, University of Colorado School of Medicine, Aurora, CO, ²Deparment of Immunology & Microbiology, University of Colorado School of Medicine, Aurora, CO, ³Center for Autoimmune Genomics and Etiology (CAGE), Division of Allergy and Immunology, Cincinnati Children's Hospital, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, ⁴Center for Autoimmune Genomics and Etiology (CAGE), Cincinnati Children's Hospital Medical Center, Cincinnati, OH, ⁵Medicine, Division of Rheumatology, University of Colorado Denver, Aurora, CO, ⁶Rheumatology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, ⁷Center for Autoimmune Genomics and Etiology (CAGE), Cincinnati Children's Hospital Medical Center; US Department of Veterans Affairs Medical Center, Cincinnati, OH
Background/Purpose: Rare variants provide important opportunity for mechanistic insight as they carry substantial effect sizes and provide deep insight into disease etiopathogenesis. To date, several…
Abstract Number: 1731 • 2017 ACR/ARHP Annual Meeting
Abnormal Responses of γδ T Cell Subsets to Stimulation with Cardiolipin and Zoledronate in Systemic Sclerosis
Ilan Bank¹, Paul Fisch², Jose Villacorta Hidalgo³, Alexandra Balbir-Gurman⁴, Yolanda Braun-Moscovici⁵ and Helena Migalovich Sheikhet⁶, ¹Medicine, Maayenei Hayeshuah and Chaim Sheba Medical Center, Israel, Bnei Brak, Israel, ²3Department of Clinical Pathology, University of Freiburg Medical Center, Freiburg, Germany, ³Department of Clinical Pathology, University of Freiburg Medical Center, Freiburg, Germany, ⁴Rheumatology Unit, Rambam Health Care Campus, Rappaport Faculty of Medicine, Technion, Haifa, Israel, Haifa, Israel, ⁵B Shine Department of Rheumatology, Rambam Health Care Campus,. Rappaport Faculty of Medicine, Technion, Haifa, Israel, ⁶Medicine, Laboratory of Immunoregulation, Chaim Sheba Medical Center, Ramat Gan, Israel
Background/Purpose: Systemic sclerosis (SSc) is an auto-immune disorder leading to destructive tissue fibrosis. Abnormal responses of SSc T cells to lipid antigens and low molecular…
Abstract Number: 1922 • 2017 ACR/ARHP Annual Meeting
Cell Type Specific Gene Expression Analysis of Early Systemic Sclerosis Skin Shows a Prominent Activation Pattern of Innate and Adaptive Immune System in the Prospective Registry for Early Systemic Sclerosis (PRESS) Cohort
Shervin Assassi¹, Dinesh Khanna², Monique Hinchcliff³, Virginia D. Steen⁴, Faye Hant⁵, Jessica K. Gordon⁶, Ami A. Shah⁷, Jun Ying⁸, William Swindell⁹, Wenjin Zheng¹⁰, Lisha Zhu¹⁰, Victoria K. Shanmugam¹¹, Robyn T. Domsic¹², Flavia V. Castelino¹³, Elana J. Bernstein¹⁴ and Tracy M. Frech¹⁵, ¹University of Texas McGovern Medical School, Houston, TX, ²University of Michigan, Ann Arbor, MI, ³Rheumatology, Northwestern Medicine, Chicago, IL, ⁴Rheumatology, MedStar Georgetown University Hospital, Washington, DC, ⁵Medicine/Rheumatology & Immunology, Medical University of South Carolina, Charleston, SC, ⁶Rheumatology, Hospital for Special Surgery, New York, NY, ⁷Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, ⁸Department of Internal Medicine - Rheumatology, University of Texas McGovern Medical School, Houston, TX, ⁹Dermatology, University of Michigan - Ann Arbor, Ann Arbor, MI, ¹⁰University of Texas - School of Biomedical Informatics, Houston, TX, ¹¹Rheumatology, The George Washington University, Washington, DC, ¹²Rheumatology, University of Pittsburgh, Pittsburgh, PA, ¹³Rheumatology, Harvard Medical School, Boston, MA, ¹⁴Rheumatology, Columbia University, New York, NY, ¹⁵Division of Rheumatology, University of Utah, Salt Lake City, UT
Background/Purpose: To examine the global gene expression profile in patients with very early diffuse systemic sclerosis (SSc). Methods: Skin biopsies were obtained from patients enrolled…
Abstract Number: 4 • 2017 Pediatric Rheumatology Symposium
Microbiota-Dependent Signals Regulate Inflammatory Myelopoiesis in a Murine Model of Macrophage Activation Syndrome
Lehn K. Weaver¹, Chhanda Biswas¹, Niansheng Chu¹ and Edward M. Behrens², ¹Pediatric Rheumatology, Children's Hospital of Philadelphia, Philadelphia, PA, ²Rheumatology, Children's Hospital of Philadelphia, Philadelphia, PA
Background/Purpose: Targeting host-microbiota interactions to limit production of pathogenic myeloid cells that fuel chronic inflammatory responses is of therapeutic interest. Recent evidence suggests that this may…
Abstract Number: 10 • 2017 Pediatric Rheumatology Symposium
Severe Juvenile Arthritis Associated with a De Novo Gain-of-Function Germline Mutation in MYD88
Keith A. Sikora¹, Joshua R. Bennett¹, Zuoming Deng², Wanxia Li Tsai³, April D. Brundidge³, Fatemeh Navid³, Gerlinde Layh-Schmitt³, Eric Hanson⁴, Massimo G. Gadina⁵, Louis M. Staudt⁶, Thomas A. Griffin⁷ and Robert Colbert³, ¹Pediatric Translational Research Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, ²Biodata Mining & Discovery, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, ³National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, ⁴Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, ⁵Translational Immunology, Office of Science and Technology, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, ⁶National Cancer Institute, National Institutes of Health, Bethesda, MD, ⁷Levine Children’s Hospital at Carolinas Medical Center, Charlotte, NC
Background/Purpose: Myeloid differentiation primary response 88 (MyD88) is a critical adaptor protein that connects Toll-like and IL-1 receptor signaling to activation of NF-κB. Germline loss-of-function…

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