Abstracts tagged "galectin"

Abstract Number: 349 • 2014 ACR/ARHP Annual Meeting
Galectin-3 in the Systemic Circulation Is Increased in Newly Diagnosed Rheumatoid Arthritis and Is Associated with Anti-CCP and Bone Marrow Edema
Saida Farah Issa¹, Anne Friesgaard Christensen², Hanne M. Lindegaard¹, Merete Lund Hetland³, Kim Hoerslev-Petersen⁴, Kirsten Junker⁵, Kristian Stengaard-Pedersen⁶, Tine Lottenburger², Torkell Ellingsen¹, Ib Hansen⁷, Jens Kristian Pedersen¹, Ulrik B. Lauridsen⁸, Anders Svendsen⁹, Ulrik Tarp⁶, Jan Pødenphant¹⁰, Mikkel Østergaard¹¹ and Peter Junker¹, ¹Department of Rheumatology, Odense University Hospital, Odense, Denmark, ²Department of Rheumatology, Vejle Hospital, Vejle, Denmark, ³DANBIO, Center for Rheumatology and Spine Diseases, Glostrup Univ Hospital, Glostrup, Denmark, ⁴Rheumatology, Research Unit at King Christian X Hospital for Rheumatic Diseases, Graasten, Denmark, ⁵Institute of Molecular Medicine, Cardiovascular & Renal Research, University of Southern Denmark, Odense, Denmark, ⁶Department of Rheumatology, Aarhus University Hospital, Aarhus, Denmark, ⁷Rheumatology, Department of Rheumatology, Aarhus University Hospital, Aarhus, Denmark, ⁸Department of Rheumatology, Copenhagen Center for Arthritis Research, Center for Rheumatology and Spine Diseases, Glostrup Hospital, Glostrup, Denmark, ⁹University of Southern Denmark, The Danish Twin Registry, Epidemiology, Institute of Public Health, Odense, Denmark, ¹⁰Department of Rheumatology, Copenhagen University Hospital at Gentofte, Gentofte, Denmark, ¹¹Center for Rheumatology and Spine Diseases, Glostrup Hospital, Copenhagen Center for Arthritis Research, Center for Rheumatology and Spine Diseases, Glostrup Hospital, Glostrup, Denmark
Background/Purpose: Galectin-3 (Gal-3), a 26kD beta-galactoside binding protein, has been implicated as a pro-inflammatory mediator in animal arthritis and rheumatoid arthritis (RA) in humans. Thus,…
Abstract Number: 630 • 2013 ACR/ARHP Annual Meeting
Galectin-3-Binding Protein Is Highly Increased On Circulating Microparticles In SLE Patients and Co-Localizes With IgG In Glomerular Deposits In Human Lupus Nephritis
Christoffer T. Nielsen^1,2, Ole Østergaard³, Ole Petter Rekvig⁴, Gunnar K. Sturfelt⁵, Søren Jacobsen⁶ and Niels H. H. Heegaard⁷, ¹Department of Clinical Biochemistry, Immunology & Genetics, Statens Serum Institut, Copenhagen S, Denmark, ²Infectious Diseases and Rheumatology, University Hospital Rigshospitalet, Copenhagen, Denmark, ³Department of Clinical Biochemistry, Immunology & Genetics, Statens Serum Institute, Copenhagen S, Denmark, ⁴Department of Biochemistry and Medical Biology, University Hospital, Tromsø, Norway, ⁵Department of Rheumatology, University Hospital Lund, Lund, Sweden, ⁶Department of Rheumatology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark, ⁷Department of Clinical Biochemistry, Immunology & Genetics, Statens Serum Institut, Copenhagen, Denmark
Background/Purpose: The origin of autoantigens in glomerular immune complex (IC) deposits in lupus nephritis patients is unknown. They may derive from the circulation (microparticle (MP)-ICs…
Abstract Number: 680 • 2012 ACR/ARHP Annual Meeting
Plasma Level of Galectin-3 Binding Protein Reflects Type I Interferon Activity and Is Highly Increased in Patients with Systemic Lupus Erythematosus
Christoffer T. Nielsen¹, Ole Østergaard², Line V. Iversen³, Christian Lood⁴, Anders A. Bengtsson⁴, Anne Voss⁵, Søren Jacobsen⁶ and Niels H. H. Heegaard³, ¹Department of Clinical Biochemistry, Immunology & Genetics, Statens Serum Institut, Copenhagen S, Denmark, ²Department of Clinical Biochemistry, Immunology & Genetics, Statens Serum Institute, Copenhagen S, Denmark, ³Department of Clinical Biochemistry, Immunology & Genetics, Statens Serum Institut, Copenhagen, Denmark, ⁴Department of Clinical Sciences, Section of Rheumatology, Lund University, Lund, Sweden, ⁵Dept of Rheumatology, Odense University Hospital, Odense C, Denmark, ⁶Department of Rheumatology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark
Background/Purpose: Ongoing production of type I interferons (IFN) is a key element in the pathogenesis of systemic lupus erythematosus (SLE). Type I IFNs trigger the…

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