interferons and mouse model Archives

Abstract Number: 40 • ACR/ARHP Annual Meeting 2018
IFN Regulatory Factor 3 but Not IFN Regulatory Factor 7 Contributes to Bone Erosion in Collagen Induced Arthritis
Susan Sweeney¹, David L. Boyle², Yuya Fujita³, Anthony Bui⁴, Gary S. Firestein² and Maripat Corr⁵, ¹Lilly Research Laboratories, Eli Lily, San Diego, CA, ²Medicine, University of California San Diego, La Jolla, CA, ³Medicine, University of California San Diego, La jolla, CA, ⁴Medicine, University of California San Diego, San Diego, CA, ⁵University of California San Diego, La Jolla, CA
Background/Purpose: Type I interferons and their mRNA signatures have become prominent in biomarkers of autoimmune and autoinflammatory disease activity. Two master regulators of type I…
Abstract Number: 1773 • ACR/ARHP Annual Meeting 2015
Pan JAK Inhibitor Tofacitinib Ameliorate Autoimmunity and Nephritis in Lupus Prone Mice Via Inhibition of Interferon Signaling Pathway
Keigo Ikeda^1,2, Kunihiro Hayakawa², Maki Fujishiro³, Mikiko Kawasaki³, Takuya Hirai^2,4, Shinji Morimoto^2,4, Yoshinari Takasaki⁵ and Iwao Sekigawa^3,4, ¹Department of Internal Medicine and Rheumatology, Juntendo University Urayasu Hospital, Tomioka, Urayasu, Chiba, Japan, ²Institute for Environmental and Gender Specific Medicine, Juntendo University Graduate School of Medicine, Chiba, Japan, ³Institute for Environment and Gender Specific Medicine, Juntendo University Graduate School of Medicine, Chiba, Japan, ⁴Department of Internal Medicine and Rheumatology, Juntendo University Urayasu Hospital, Chiba, Japan, ⁵Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan
Background/Purpose: We previously reported that Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway-mediated regulation of interferon (IFN) regulatory factor (IRF)-related genes may have an…
Abstract Number: 2870 • ACR/ARHP Annual Meeting 2014
B Cell-Intrinsic Deletion of the Type 1 Interferon Receptor Does Not Impact the Development of Murine Lupus
Shaun W. Jackson^1,2, Nicole Scharping¹, Socheath Khim¹ and David Rawlings^1,2, ¹Seattle Children's Research Institute, Seattle, WA, ²Pediatrics, University of Washington, Seattle, WA
Background/Purpose Type 1 interferon (IFN) is strongly implicated in lupus pathogenesis, and patients with SLE frequently express a “type 1 IFN gene signature”. Type 1…
Abstract Number: 2895 • ACR/ARHP Annual Meeting 2013
Bacterial Amyloids Promote Type I Interferon Production and Accelerate Autoimmunity
Paul Gallo, Glenn Rapsinski, Cagla Tukel and Stefania Gallucci, Dept. of Microbiology and Immunology, Laboratory of Dendritic Cell Biology, Temple Autoimmunity Center, Temple University School of Medicine, Philadelphia, PA
Background/Purpose: Infection is a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). This is largely due to the use of…
Abstract Number: 2737 • ACR/ARHP Annual Meeting 2013
In Vivo MiR-146a Administration Ameliorates Murine Lupus Nephritis
Dong Liang¹, Shiyu Zhou², Zheng Liu³, Zhengyuan Shan¹, Philip Brohawn³, Yihong Yao³, Indu Raman⁴, Quan-Zhen Li⁴, John B. Harley^5,6 and Nan Shen^1,2,7, ¹Division of Rheumatology & the Center for Autoimmune Genomics and Etiology (CAGE), Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, ²Shanghai Institutes for Biological Sciences Chinese Academy of Sciences & Shanghai Jiao Tong University School of Medicine, Shanghai, China, ³Translational Sciences, MedImmune, LLC, Gaithersburg, MD, ⁴Department of Immunology and Microarray Core Facility, University of Texas Southwestern Medical Center, Dallas, TX, ⁵Division of Rheumatology and The Center for Autoimmune Genomics & Etiology, University of Cincinnati, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, ⁶US Department of Veterans Affairs Medical Center, Cincinnati, OH, ⁷Shanghai Institute of Rheumatology, Shanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
Background/Purpose: New Zealand black and white F1 (NZBW/F1) is a classic mouse model of systemic lupus erythematosus (SLE). Type I interferon (IFN) infusion accelerates lupus…
Abstract Number: 2722 • ACR/ARHP Annual Meeting 2013
In Vivo Administration Of MiR-146a Protects C57BL/6 Mice From Pristane-Induced Pulmonary Hemorrhage Via Suppressing Type I Interferon Response
Dong Liang¹, Shiyu Zhou², Zheng Liu³, Zhengyuan Shan¹, Philip Brohawn³, Yihong Yao³, John B. Harley^4,5 and Nan Shen^1,2,6, ¹Division of Rheumatology & the Center for Autoimmune Genomics and Etiology (CAGE), Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, ²Shanghai Institutes for Biological Sciences Chinese Academy of Sciences & Shanghai Jiao Tong University School of Medicine, Shanghai, China, ³Translational Sciences, MedImmune, LLC, Gaithersburg, MD, ⁴Division of Rheumatology and The Center for Autoimmune Genomics & Etiology, University of Cincinnati, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, ⁵US Department of Veterans Affairs Medical Center, Cincinnati, OH, ⁶Shanghai Institute of Rheumatology, Shanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
Background/Purpose: miR-146a as an endogenous regulator plays a critical role in resolving acute inflammation. The risk-associated genetic variant in miR-146a promoter was linked to reduced…

Abstracts tagged "interferons and mouse model"

IFN Regulatory Factor 3 but Not IFN Regulatory Factor 7 Contributes to Bone Erosion in Collagen Induced Arthritis

Pan JAK Inhibitor Tofacitinib Ameliorate Autoimmunity and Nephritis in Lupus Prone Mice Via Inhibition of Interferon Signaling Pathway

B Cell-Intrinsic Deletion of the Type 1 Interferon Receptor Does Not Impact the Development of Murine Lupus

Bacterial Amyloids Promote Type I Interferon Production and Accelerate Autoimmunity

In Vivo MiR-146a Administration Ameliorates Murine Lupus Nephritis

In Vivo Administration Of MiR-146a Protects C57BL/6 Mice From Pristane-Induced Pulmonary Hemorrhage Via Suppressing Type I Interferon Response