PMID: 15230282Jul 3, 2004Paper

New insights into complement: a mediator of injury and marker of disease activity in systemic lupus erythematosus

Lupus
S ManziJ Salmon

Abstract

Studies performed during the past several decades have demonstrated a role for the complement system in both the etiology and pathogenesis of systemic lupus erythematosus (SLE). However the specifically defective molecular and cellular pathways responsible for the disease and its complications have generally not been identified. In this report, we describe two recent advances in complement pathobiology that highlight future directions for promising investigation toward enhancing our capacity to diagnose SLE, to monitor activity of the disease, and to identify molecular and cellular defects in SLE that can be targeted by therapeutic inhibitors of complement activation. In the first example, we describe recently developed assays to detect erythrocyte C4d and complement receptor 1 for diagnosis and monitoring of disease activity in SLE. In the second example, we describe a recently discovered role for complement in mediating fetal loss in antiphospholipid syndrome and discuss the potential for this observation to facilitate identification and development of complement based biomarkers to predict poor fetal outcome in pregnant patients with SLE. These two examples are meant to underscore the importance of complement in the etiology...Continue Reading

References

Jan 1, 1992·Annals of the Rheumatic Diseases·C K Ting, K H Hsieh
Dec 1, 1991·American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation·D M RickerJ D Clough
Feb 1, 1989·Annals of the Rheumatic Diseases·J A CharlesworthD Wakefield
Feb 1, 1988·Arthritis and Rheumatism·M J Walport, P J Lachmann
May 1, 1986·Annals of the Rheumatic Diseases·A J SwaakW Bronsveld
Dec 1, 1986·Arthritis and Rheumatism·M D LockshinP C Harpel
Jan 1, 1985·Scandinavian Journal of Rheumatology·G SturfeltA G Sjöholm
Dec 1, 1967·The Journal of Clinical Investigation·C A Alper, F S Rosen
Jan 1, 1984·International Archives of Allergy and Applied Immunology·G Sturfelt, A G Sjöholm
Jul 1, 1982·Arthritis and Rheumatism·P H Schur
Mar 1, 1995·Clinical Immunology and Immunopathology·J M PorcelD Vergani
Nov 18, 2000·Advances in Immunology·M C PickeringM J Walport
Dec 21, 2000·Current Rheumatology Reports·J S Navratil, J M Ahearn
Jun 21, 2001·Immunological Reviews·R BarringtonM C Carroll
Jan 24, 2002·The Journal of Experimental Medicine·V Michael HolersJane E Salmon
Dec 24, 2002·Current Opinion in Rheumatology·Maria-Louise Barilla-LaBarca, John P Atkinson

❮ Previous
Next ❯

Citations

Oct 10, 2007·Rheumatology International·Antoni Hrycek, Urszula Siekiera
Nov 3, 2011·Nature Reviews. Rheumatology·Maria G Tektonidou, Michael M Ward
Mar 28, 2008·Expert Review of Molecular Diagnostics·Chang-Hee Suh, Hyoun-Ah Kim
Mar 6, 2010·Rheumatic Diseases Clinics of North America·Anup Manoharan, Michael P Madaio
Sep 20, 2005·Trends in Immunology·Jennifer A Croker, Robert P Kimberly
Feb 22, 2018·International Journal of Molecular Sciences·Lorena Alvarez-RodriguezVictor Martínez-Taboada
Mar 22, 2019·Frontiers in Immunology·Lorena Álvarez-RodríguezMarcos López-Hoyos

❮ Previous
Next ❯

Related Concepts

Related Feeds

Antiphospholipid Syndrome

Antiphospholipid syndrome or antiphospholipid antibody syndrome (APS or APLS), is an autoimmune, hypercoagulable state caused by the presence of antibodies directed against phospholipids.