Abstracts tagged "interferons and toll-like receptors"

Abstract Number: 97 • 2018 ACR/ARHP Annual Meeting
Enhanced IFN-α Production By Plasmacytoid Dendritic Cells Is Associated with Increased Toll-like Receptor 7 Retention in the Lysosomes and Exosure to Type I IFN in Systemic Lupus Erythematosus
Goh Murayama¹, Asako Chiba², Ayako Makiyama², Ken Yamaji¹, Naoto Tamura¹ and Sachiko Miyake², ¹Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan, ²Immunology, Juntendo University School of Medicine, Tokyo, Japan
Background/Purpose: Type I interferon(IFN) appears to contribute to the development of systemic lupus erythematosus (SLE). Overexpression of type I IFN regulated genes has been reported…
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: 1829 • 2016 ACR/ARHP Annual Meeting
Hyper-Responsiveness to TLR-4 Stimulation in SLE: Association with High Levels of Serum IFN-Alpha and a Distinct Inflammatory Cytokine Profile
Uma Thanarajasingam¹, Mark A. Jensen², Jessica M. Dorschner³, Danielle Vsetecka³, Shreyasee Amin⁴, Ashima Makol⁴, Floranne C. Ernste⁵, Thomas Osborn⁴, Vaidehi Chowdhary⁴ and Timothy B. Niewold⁶, ¹Division of Rheumatology, Mayo Clinic, Rochester, MN, ²Department of Immunology and Division of Rheumatology, Mayo Clinic, Rochester, MN, ³Division of Rheumatology and Department of Immunology, Mayo Clinic, Rochester, MN, ⁴Rheumatology, Mayo Clinic, Rochester, MN, ⁵Division of Rheumatology, Mayo Clinic Rochester, Rochester, MN, ⁶Rheumatology and Immunology, Mayo Clinic, Rochester, MN
Background/Purpose: IFN-alpha is a pathogenic factor in SLE. High serum interferon activity (IFN-high) marks a subgroup of SLE patients strongly associated with double-stranded DNA (dsDNA) antibodies.…
Abstract Number: 1754 • 2015 ACR/ARHP Annual Meeting
BANK1 Controls the Development of SLE By Modulating TLR7 Signaling and Type I IFN-Induced Translation Initiation Pathway in B Cells
Ying-Yu Wu¹, Ramesh Kumar², Harini Bagavant¹ and Marta E. Alarcon Riquelme³, ¹Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation, Oklahoma City, OK, ²Oklahoma Medical Research Foundation, Oklahoma Cty, OK, ³Arthritis & Clinical Immunology, Oklahoma Medical Research Foundation, Center for Genomics and Oncological Research Pfizer-University of Granada-Junta de Andalucia, Oklahoma City, OK
Background/Purpose: BANK1 is a susceptibility gene for SLE, and we have shown that stimulation of TLR9 agonist leads to a reduction in the activation of…
Abstract Number: 1813 • 2015 ACR/ARHP Annual Meeting
Novel Mechanism of Action of Anti-Malarial Drugs in the Inhibition of Type I Interferon Production
Jie An¹, Joshua Woodward², Mark Minie³, YuFeng Peng⁴, Tomikazu Sasaki⁵ and Keith B. Elkon⁶, ¹Division of Rheumatology, Department of Medicine & Immunology, University of Washington, Seattle, WA, ²Department of Microbiology, University of Washington, Seattle, WA, ³Department of Bioengineering, University of Washington, Seattle, WA, ⁴Rheumatology, University of Washington, Seattle, WA, ⁵Department of Chemistry, University of Washington, Seattle, WA, ⁶Department of Medicine & Immunology, University of Washington, Seattle, WA
Background/Purpose: Anti-malarial drugs (AMD) such as Hydroxychloroquine (HCQ) and Quinacrine (QC) are effective in the treatment of skin rash and arthritis in systemic lupus erythematosus…
Abstract Number: 3024 • 2015 ACR/ARHP Annual Meeting
FcÎ³riiia Mediated Signal Cause Epigenetic Changes in Human Naive CD4+ T-Cells
Ye Bi¹, Chen Chen², Terry Moore³ and Anil K. Chauhan⁴, ¹Internal Medicine, Saint Louis University, St. Louis, MO, ²Biostatistics and Epidemiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, ³Division of Rheumatology and Pediatric Rheumatology, Saint Louis University School of Medicine, St Louis, MO, ⁴Internal Medicine-Rheumatology, Saint Louis University, St Louis, MO
Background/Purpose: Signals that trigger epigenetic changes in CD4+ T-cells are unknown. To examine a role for FcγRIIIa mediated co-signal in causing epigenetic changes in human…
Abstract Number: 1614 • 2014 ACR/ARHP Annual Meeting
Functional Analysis of Interferon Responsiveness in PBMC from SLE Donors Identifies Subgroups with Higher and Lower Disease Activity
Rachael Hawtin¹, Wouter Korver², Erik Evensen², Diane Longo², Drew Hotson², Nikil Wale², Andy Conroy², Alessandra Cesano², Barbara Mittleman², Tsung Lin³, Vikram R. Rao⁴, Elena Peeva⁵, Stephen Benoit⁵, Martin Hodge³, James D. Clark³, Aaron R. Winkler⁶ and Jean-Baptiste Telliez³, ¹Nodality Inc., South San Francisco, CA, ²Nodality, Inc., South San Francisco, CA, ³Immunoscience, Pfizer Biotherapeutics Research and Development, Cambridge, MA, ⁴Inflammation & Remodeling, Pfizer, Cambridge, MA, ⁵Precision Medicine, Pfizer Biotherapeutics Research and Development, Cambridge, MA, ⁶Inflammation and Remodeling, Pfizer Biotherapeutics Research and Development, Cambridge, MA
Background/Purpose: Interferons (IFN) reportedly are central to SLE pathogenesis and increased expression of IFN regulated genes (the ‘IFN signature') is associated with active disease. Clinical…

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