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Journal of Biomedicine and Biotechnology
Volume 2010, Article ID 607084, 13 pages
Review Article

Accelerated Atherosclerosis in Systemic Lupus Erythematosus: Role of Proinflammatory Cytokines and Therapeutic Approaches

1Unidad de Investigación, Hospital Universitario Reina Sofia, Instituto de Investigacion Biomédica de Córdoba (IMIBIC), E-14004 Córdoba, Spain
2Hospital Virgen de la Victoria, Fundación IMABIS, E-29010 Málaga, Spain
3Lupus Research Unit, St Thomas Hospital, London SE1 7EH, UK

Received 15 January 2010; Revised 21 June 2010; Accepted 26 July 2010

Academic Editor: Timothy B. Niewold

Copyright © 2010 Chary López-Pedrera et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Systemic lupus erythematosus (SLE), a chronic multisystem autoimmune disease with a broad range of clinical manifestations, is associated with accelerated atherosclerosis (AT) and increased risk of cardiovascular complications. Relevant factors directly influencing the development of AT comprise immune complex generation, complement activation, and changes in the production and activity of a complex network of cytokines, including type I and II interferons, B lymphocyte stimulator (BLyS), TNF , IL-6, IL-17 and migration macrophage inhibitor (MIF). Autoantibodies, also responsible for cytokine expression and activation, play a supplementary key role in the development of AT. Genomic and proteomic studies have contributed to the discovery of genes and proteins involved in AT, including some that may be suitable to be used as biomarkers. All that data has allowed the development of new drugs, most of them evaluated in clinical trials: inhibitors of IFN and TNF , B cell directed therapies, synthetic oligodeoxynucleotides, intravenous immunoglobulin, or statins. The focus of the present paper is to summarize recent evidence showing the role of cytokines in the development of AT in SLE and the rationale, and safety concerns, in the use of combined therapy to prevent AT and cardiovascular disease.