Journal article
New insights into complement: a mediator of injury and marker of disease activity in systemic lupus erythematosus
Lupus, v 13(5), pp 298-303
01 Jan 2004
PMID: 15230282
Featured in Collection : UN Sustainable Development Goals @ Drexel
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 and pathogenesis of SLE and its complications, and to stress the need for further investigation focused on the link between the complement system and SLE.
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Details
- Title
- New insights into complement: a mediator of injury and marker of disease activity in systemic lupus erythematosus
- Creators
- S Manzi - University of PittsburghJ M Ahearn - University of PittsburghJ Salmon - Hospital for Special Surgery
- Publication Details
- Lupus, v 13(5), pp 298-303
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Medicine (Graduate); General Internal Medicine
- Web of Science ID
- WOS:000222152800003
- Scopus ID
- 2-s2.0-2942715102
- Other Identifier
- 991021934013504721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Rheumatology