Abstracts tagged "autoimmune diseases and interferons"

Abstract Number: 93 • 2019 ACR/ARP Annual Meeting
Interferon Pathway Activation in T Follicular Helper (Tfh) Cell Subsets in Human Myositis
Amrutesh Puranik¹, Mark Jensen ², Regine Tipon ³, Yogita Ghodke-Puranik ³, Valeria Mezzano ⁴, Shanmugapriya Selvaraj ⁵, Theresa Wampler Muskardin ⁴, Cynthia Loomis ⁴, Ann Reed ⁶, Lauren Pachman ⁷ and Timothy Niewold ⁵, ¹NYU Langone Health, New York, NY, ²Colton Center for Autoimmunity, NYU School of Medicine, New York, NY, ³Colton Center for Autoimmunity, NYU School of Medicine, New York, ⁴New York University Langone Health, New York, ⁵New York University Langone Health, New York, NY, ⁶Duke University School of Medicine, Durham, NC, ⁷Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, IL
Background/Purpose: T and B cells come together in ectopic lymphoid aggregates in myositis, suggesting that local T:B cell interactions could play a role in disease. …
Abstract Number: 1843 • 2016 ACR/ARHP Annual Meeting
Single Cell Expression Quantitative Trait Loci (eQTL) Analysis of Established SLE-Risk Loci in Lupus Patient Monocytes
Yogita Ghodke-Puranik¹, Zhongbo Jin¹, Wei Fan², Mark A. Jensen³, Jessica M. Dorschner¹, Danielle Vsetecka¹, Shreyasee Amin⁴, Ashima Makol⁴, Floranne C. Ernste⁵, Thomas Osborn⁴, Kevin Moder⁴, Vaidehi Chowdhary⁴ and Timothy B. Niewold⁶, ¹Division of Rheumatology and Department of Immunology, Mayo Clinic, Rochester, MN, ²Department of Rheumatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, China, Shanghai, China, ³Department of Immunology and Division of Rheumatology, Mayo Clinic, Rochester, MN, ⁴Rheumatology, Mayo Clinic, Rochester, MN, ⁵Division of Rheumatology, Mayo Clinic, Rochester, MN, ⁶Rheumatology and Immunology, Mayo Clinic, Rochester, MN
Background/Purpose: While most of the confirmed SLE-risk loci are in or near genes with immune system function, a major unanswered question is how these loci…
Abstract Number: 2984 • 2016 ACR/ARHP Annual Meeting
Novel Anti-Malarial Drug Derivative Inhibited Type I Interferon Production and Autoimmune Inflammation through Inhibition of CGAS-Sting Pathway in Trex1-/- Mouse
Jie An¹, Joshua Woodward², Mark Minie³, Xizhang Sun⁴, Lena Tanaka¹, Yufeng Peng¹, Jessica Snyder⁴, Tomikazu Sasaki⁵ and Keith B. Elkon⁶, ¹Division of Rheumatology, University of Washington, Seattle, WA, ²Department of Microbiology, University of Washington, Seattle, WA, ³Department of Bioengineering, University of Washington, Seattle, WA, ⁴University of Washington, Seattle, WA, ⁵Department of Chemistry, University of Washington, Seattle, WA, ⁶Department of Medicine, Division of Rheumatology, University of Washington, Seattle, WA
Background/Purpose: Type I interferon, (IFN-I) is strongly implicated in the pathogenesis of SLE as well as rare monogenic ‘interferonopathies’ such as Aicardi-Goutieres Syndrome (AGS) caused…
Abstract Number: 1376 • 2015 ACR/ARHP Annual Meeting
Presence of the Interferon Signature in Anti-Nuclear Antibody Positive Individuals Prior to the Onset of Systemic Autoimmune Rheumatic Disease
Joan Wither¹, Tony Liu¹, Babak Noamani², Dennisse Bonilla¹, Sindhu R. Johnson³, Earl Silverman⁴, Arthur Bookman¹, Larissa Lisnevskaia⁵ and Carolina Landolt-Marticorena¹, ¹University Health Network, Toronto, ON, Canada, ²Genetics and developmental biology, University Health Network, Toronto, ON, Canada, ³Toronto Scleroderma Program, Toronto Western Hospital, Mount Sinai Hospital, University of Toronto, University Health Network Pulmonary Hypertension Programme, Toronto, ON, Canada, ⁴The Hospital for Sick Children, Toronto, ON, Canada, ⁵Lakeridge Health Services, Oshawa, ON, Canada
Background/Purpose: Patients with systemic autoimmune rheumatic diseases (SARD) often have a prolonged pre-clinical phase during which they are anti-nuclear antibody (ANA)+ but lack clinical symptoms. …
Abstract Number: 233 • 2012 ACR/ARHP Annual Meeting
IFN Signature Is Associated with Autoantibody Profiles in Patients with Idiopathic Inflammatory Myopathies
Saskia Vosslamber¹, Louise Ekholm², Anna Tjarnlund³, Clio P. Mavragani⁴, Lenka Plestilova⁵, Martin Klein⁶, Mary K. Crow⁷, Peter J. Charles⁸, Leonid Padyukov⁹, Jiri Vencovsky⁵, Ingrid E. Lundberg¹⁰ and Cornelis L. Verweij¹, ¹Pathology, VU University Medical Center, Amsterdam, Netherlands, ²Rheumatology Unit, Department of Medicine, Karolinska University Hospital in Solna, Karolinska Institutet, Stockholm, Sweden, ³Pathology, Rheumatology Unit, Department of Medicine, Karolinska University Hospital in Solna, Karolinska Institutet, Stockholm, Sweden, ⁴Department of Experimental Physiology, School of Medicine, University of Athens, Athens, Greece, Athens, Greece, ⁵Institute of Rheumatology, Prague, Czech Republic, ⁶Institute of Rheumatology, Prague, Prague, Czech Republic, ⁷Department of Medicine, Hospital for Special Surgery, New York, NY, ⁸Oxford University, Kennedy Institute of Rheumatology, Oxford, United Kingdom, ⁹Rheumatology Unit, Karolinska Institutet, Stockholm, Sweden, ¹⁰Rheumatology Unit, Rheumatology Unit, Department of Medicine, Karolinska University Hospital, Solna, Karolinska Institutet, Sweden, Stockholm, Sweden
Background/Purpose: Idiopathic inflammatory myopathies (IIM) are rare autoimmune diseases characterized by the presence of autoantibodies, proximal muscle weakness and muscle inflammation. Recent studies showed an…

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